112 results on '"Hadoke, P W"'
Search Results
2. Correction: Autophagy protein 5 controls flow-dependent endothelial functions
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Nivoit, Pierre, Mathivet, Thomas, Wu, Junxi, Salemkour, Yann, Sankar, Devanarayanan Siva, Baudrie, Véronique, Bourreau, Jennifer, Guihot, Anne-Laure, Vessieres, Emilie, Lemitre, Mathilde, Bocca, Cinzia, Teillon, Jérémie, Le Gall, Morgane, Chipont, Anna, Robidel, Estelle, Dhaun, Neeraj, Camerer, Eric, Reynier, Pascal, Roux, Etienne, Couffinhal, Thierry, Hadoke, Patrick W. F., Silvestre, Jean-Sébastien, Guillonneau, Xavier, Bonnin, Philippe, Henrion, Daniel, Dengjel, Joern, Tharaux, Pierre-Louis, and Lenoir, Olivia
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- 2023
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3. Autophagy protein 5 controls flow-dependent endothelial functions
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Nivoit, Pierre, Mathivet, Thomas, Wu, Junxi, Salemkour, Yann, Sankar, Devanarayanan Siva, Baudrie, Véronique, Bourreau, Jennifer, Guihot, Anne-Laure, Vessieres, Emilie, Lemitre, Mathilde, Bocca, Cinzia, Teillon, Jérémie, Le Gall, Morgane, Chipont, Anna, Robidel, Estelle, Dhaun, Neeraj, Camerer, Eric, Reynier, Pascal, Roux, Etienne, Couffinhal, Thierry, Hadoke, Patrick W. F., Silvestre, Jean-Sébastien, Guillonneau, Xavier, Bonnin, Philippe, Henrion, Daniel, Dengjel, Joern, Tharaux, Pierre-Louis, and Lenoir, Olivia
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- 2023
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4. Generation of a Novel In Vitro Model to Study Endothelial Dysfunction from Atherothrombotic Specimens
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Gallogly, Susan, Fujisawa, Takeshi, Hung, John D., Brittan, Mairi, Skinner, Elizabeth M., Mitchell, Andrew J., Medine, Claire, Luque, Neus, Zodda, Erika, Cascante, Marta, Hadoke, Patrick W., Mills, Nicholas L., and Tura-Ceide, Olga
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- 2021
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5. WT1 expression in vessels varies with histopathological grade in tumour-bearing and control tissue from patients with breast cancer
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McGregor, Richard J., Chau, You-Ying, Kendall, Timothy J., Artibani, Mara, Hastie, Nicholas, and Hadoke, Patrick W. F.
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- 2018
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6. Leukemia Inhibitory Factor-Receptor is Dispensable for Prenatal Testis Development but is Required in Sertoli cells for Normal Spermatogenesis in Mice
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Curley, Michael, Milne, Laura, Smith, Sarah, Atanassova, Nina, Rebourcet, Diane, Darbey, Annalucia, Hadoke, Patrick W. F., Wells, Sara, and Smith, Lee B.
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- 2018
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7. PET Cell Tracking Using 18F-FLT is Not Limited by Local Reuptake of Free Radiotracer
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MacAskill, Mark G., Tavares, Adriana S., Wu, Junxi, Lucatelli, Christophe, Mountford, Joanne C., Baker, Andrew H., Newby, David E., and Hadoke, Patrick W. F.
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- 2017
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8. Modulation of 11β-Hydroxysteroid Dehydrogenase as a Strategy to Reduce Vascular Inflammation
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Hadoke, Patrick W. F., Kipari, Tiina, Seckl, Jonathan R., and Chapman, Karen E.
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- 2013
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9. Obesity-induced mesenteric PVAT remodelling is sexually dimorphic, but not driven by ovarian hormones: Short title: Obesity induces sex-specific responses in mesenteric PVAT
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Ivatt, Lisa, Paul, Mhairi, Miguelez-Crespo, Allende, Hadoke, Patrick W. F., Bailey, Matthew A., Morgan, Ruth A., and Nixon, Mark
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- 2025
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10. Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function
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Hadoke, P. W. F., Macdonald, L., Logie, J. J., Small, G. R., Dover, A. R., and Walker, B. R.
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- 2006
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11. Physiological roles of glucocorticoids during early embryonic development of the zebrafish (Danio rerio)
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Wilson, K. S., Matrone, G., Livingstone, D. E. W., Al-Dujaili, E. A. S., Mullins, J. J., Tucker, C. S., Hadoke, P. W. F., Kenyon, C. J., and Denvir, M. A.
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- 2013
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12. Granulocyte colony-stimulating factor (G-CSF) depresses angiogenesis in vivo and in vitro: implications for sourcing cells for vascular regeneration therapy
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Tura, O., Crawford, J., Barclay, G. R., Samuel, K., Hadoke, P. W. F., Roddie, H., Davies, J., and Turner, M. L.
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- 2010
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13. The endothelin system as a therapeutic target in cardiovascular disease: great expectations or bleak house?
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Kirkby, N S, Hadoke, P W F, Bagnall, A J, and Webb, D J
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- 2008
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14. Enhanced endothelium derived hyperpolarising factor activity in resistance arteries from normal pressure glaucoma patients: implications for vascular function in the eye
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Cleary, C, Buckley, C H, Henry, E, McLoughlin, P, O’Brien, C, and Hadoke, P W F
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- 2005
15. Estrogens protect male mice from obesity complications and influence glucocorticoid metabolism
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Dakin, R S, Walker, B, Seckl, J R, Hadoke, P W F, and Drake, A J
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Inflammation ,Male ,Estrogens ,Glucose Tolerance Test ,Diet, High-Fat ,Lipid Metabolism ,Mice, Inbred C57BL ,Disease Models, Animal ,Mice ,Adipose Tissue ,Liver ,Receptors, Estrogen ,Animals ,Original Article ,Female ,Obesity ,Glucocorticoids ,hormones, hormone substitutes, and hormone antagonists ,Adiposity - Abstract
BackgroundAlthough the prevalence of obesity is higher amongst women than men, they are somewhat protected from the associated cardiometabolic consequences. The increase in cardiovascular disease risk seen after the menopause suggests a role for estrogens. There is also growing evidence for the importance of estrogen on body fat and metabolism in males. We hypothesised that that estrogen administration would ameliorate the adverse effects of obesity on metabolic parameters in males.MethodsMale and female C57Bl/6 mice were fed control (CON) or obesogenic (DIO) diets from 5 weeks of age until adulthood. Glucose tolerance testing was performed at 13 weeks. Mice were killed at 15 weeks and liver and adipose tissue collected for analysis of gene expression. A second cohort of male mice underwent the same experimental design with the addition of estradiol pellet implantation or sham surgery at 6 weeks.ResultsDIO males had greater mesenteric adipose deposition and more severe increases in plasma glucose, insulin and lipids than females. Treatment of males with estradiol from 6 weeks of age prevented DIO-induced increases in adipose tissue mass and alterations in glucose-insulin homeostasis. We also identified sex differences in the transcript levels and activity of hepatic and adipose glucocorticoid metabolising enzymes. Estrogen treatment feminised the pattern of DIO-induced changes in glucocorticoid metabolism, rendering males similar to females.ConclusionsThus, DIO induces sex-specific changes in glucose-insulin homeostasis which are ameliorated in males treated with estrogen, highlighting the importance of sex steroids in metabolism. Given that altered peripheral glucocorticoid metabolism has been observed in rodent and human obesity, our results also suggest that sexually dimorphic expression and activity of glucocorticoid metabolising enzymes may play a role in the differential metabolic responses to obesity in males and females.International Journal of Obesity accepted article preview online, 02 June 2015. doi:10.1038/ijo.2015.102.
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- 2015
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16. Endothelin-1 Mediates the Systemic and Renal Hemodynamic Effects of GPR81 Activation.
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Jones, Natalie K., Stewart, Kevin, Czopek, Alicja, Menzies, Robert I., Thomson, Adrian, Moran, Carmel M., Cairns, Carolynn, Conway, Bryan R., Denby, Laura, Livingstone, Dawn E.W., Wiseman, John, Hadoke, Patrick W., Webb, David J., Dhaun, Neeraj, Dear, James W., Mullins, John J., and Bailey, Matthew A.
- Abstract
GPR81 (G-protein-coupled receptor 81) is highly expressed in adipocytes, and activation by the endogenous ligand lactate inhibits lipolysis. GPR81 is also expressed in the heart, liver, and kidney, but roles in nonadipose tissues are poorly defined. GPR81 agonists, developed to improve blood lipid profile, might also provide insights into GPR81 physiology. Here, we assessed the blood pressure and renal hemodynamic responses to the GPR81 agonist, AZ'5538. In male wild-type mice, intravenous AZ'5538 infusion caused a rapid and sustained increase in systolic and diastolic blood pressure. Renal artery blood flow, intrarenal tissue perfusion, and glomerular filtration rate were all significantly reduced. AZ'5538 had no effect on blood pressure or renal hemodynamics in Gpr81-/- mice. Gpr81 mRNA was expressed in renal artery vascular smooth muscle, in the afferent arteriole, in glomerular and medullary perivascular cells, and in pericyte-like cells isolated from kidney. Intravenous AZ'5538 increased plasma ET-1 (endothelin 1), and pretreatment with BQ123 (endothelin-A receptor antagonist) prevented the pressor effects of GPR81 activation, whereas BQ788 (endothelin-B receptor antagonist) did not. Renal ischemia-reperfusion injury, which increases renal extracellular lactate, increased the renal expression of genes encoding ET-1, KIM-1 (Kidney Injury Molecule 1), collagen type 1-α1, TNF-α (tumor necrosis factor-α), and F4/80 in wild-type mice but not in Gpr81-/- mice. In summary, activation of GPR81 in vascular smooth muscle and perivascular cells regulates renal hemodynamics, mediated by release of the potent vasoconstrictor ET-1. This suggests that lactate may be a paracrine regulator of renal blood flow, particularly relevant when extracellular lactate is high as occurs during ischemic renal disease. [ABSTRACT FROM AUTHOR]
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- 2020
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17. Early-life perturbations in glucocorticoid activity impacts on the structure, function and molecular composition of the adult zebrafish
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Wilson, K S, Baily, J, Tucker, C S, Matrone, G, Vass, S, Moran, C, Chapman, K E, Mullins, J J, Kenyon, C, Hadoke, P W F, and Denvir, M A
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animal structures - Abstract
Background: Transient early-life perturbations in glucocorticoids (GC) are linked with cardiovascular disease risk in later life. Here the impact of early life manipulations of GC on adult heart structure, function and gene expression were assessed. Methods and results: Zebrafish embryos were incubated in dexamethasone (Dex) or injected with targetedglucocorticoid receptor (GR) morpholino knockdown (GR Mo) over the first 120 h post fertilisation (hpf); surviving embryos (>90%) were maintained until adulthood under normal conditions. Cardiac function, heart histology and cardiac genes were assessed in embryonic (120 hpf) and adult (120 days post fertilisation (dpf)) hearts. GR Mo embryos (120 hpf) had smaller hearts with fewer cardiomyocytes, less mature striation pattern, reduced cardiac function and reduced levels of vmhc and igf mRNA compared with controls. GR Mo adult hearts were smaller with diminished trabecular network pattern, reduced expression of vmhc and altered echocardiographic Doppler flow compared to controls. Dex embryos had larger hearts at 120 hpf (Dex 107.2 ± 3.1 vs. controls 90.2 ± 1.1 mm, p < 0.001) with a more mature trabecular network and larger cardiomyocytes (1.62 ± 0.13 cells/mm vs control 2.18 ± 0.13 cells/mm, p < 0.05) and enhanced cardiac performance compared to controls. Adult hearts were larger (1.02 ± 0.07 mg/mg vs controls 0.63 ± 0.06 mg/mg, p ¼ 0.0007), had increased vmhc and gr mRNA levels. Conclusion: Perturbations in GR activity during embryonic development results in short and long-term alterations in the heart.
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- 2015
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18. Early-life glucocorticoids programme behaviour and metabolism in adulthood in zebrafish
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Wilson, K S, primary, Tucker, C S, additional, Al-Dujaili, E A S, additional, Holmes, M C, additional, Hadoke, P W F, additional, Kenyon, C J, additional, and Denvir, M A, additional
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- 2016
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19. Dysregulation of Cortisol Metabolism in Equine Pituitary Pars Intermedia Dysfunction.
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Morgan, Ruth A, Keen, John A, Homer, Natalie, Nixon, Mark, McKinnon-Garvin, Anna M, Moses-Williams, Jodie A, Davis, Sarah R, Hadoke, Patrick W F, and Walker, Brian R
- Abstract
Equine Cushing disease [pituitary pars intermedia dysfunction (PPID)] is a common condition of older horses, but its pathophysiology is complex and poorly understood. In contrast to pituitary-dependent hyperadrenocorticism in other species, PPID is characterized by elevated plasma ACTH but not elevated plasma cortisol. In this study, we address this paradox and the hypothesis that PPID is a syndrome of ACTH excess in which there is dysregulation of peripheral glucocorticoid metabolism and binding. In 14 horses with PPID compared with 15 healthy controls, we show that in plasma, cortisol levels and cortisol binding to corticosteroid binding globulin were not different; in urine, glucocorticoid and androgen metabolites were increased up to fourfold; in liver, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) expression was reduced; in perirenal adipose tissue, 11β-HSD1 and carbonyl reductase 1 expression was increased; and tissue cortisol levels were not measurably different. The combination of normal plasma cortisol with markedly enhanced urinary cortisol metabolite excretion and dysregulated tissue-specific steroid-metabolizing enzymes suggests that cortisol clearance is increased in horses with PPID. We infer that the ACTH excess may be compensatory and pituitary pathology and autonomous secretion may be a secondary rather than primary pathology. It is possible that successful therapy in PPID may be targeted either at lowering ACTH or, paradoxically, at reducing cortisol clearance.
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- 2018
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20. Endothelium-derived hyperpolarizing factor and potassium use different mechanisms to induce relaxation of human subcutaneous resistance arteries
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McIntyre, C-A, Buckley, C H, Jones, G C, Sandeep, T C, Andrews, R C, Elliott, A I, Gray, G A, Williams, B C, McKnight, J A, Walker, B R, and Hadoke, P W F
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Adult ,Male ,Time Factors ,Charybdotoxin ,Vasodilator Agents ,Barium Compounds ,Indomethacin ,In Vitro Techniques ,Nitroarginine ,Biological Factors ,Norepinephrine ,Chlorides ,Humans ,Enzyme Inhibitors ,Ouabain ,Aged ,Skin ,Dose-Response Relationship, Drug ,Arteries ,Middle Aged ,Acetylcholine ,Vasodilation ,Apamin ,Papers ,Potassium ,Female ,Endothelium, Vascular ,Nitric Oxide Synthase - Abstract
This investigation examined the hypothesis that release of K(+) accounts for EDHF activity by comparing relaxant responses produced by ACh and KCl in human subcutaneous resistance arteries. Resistance arteries (internal diameter 244+/-12 microm, n=48) from human subcutaneous fat biopsies were suspended in a wire myograph. Cumulative concentration-response curves were obtained for ACh (10(-9) - 3x10(-5) M) and KCl (2.5 - 25 mM) following contraction with noradrenaline (NA; 0.1 - 3 microM). ACh (E(max) 99.07+/-9.61%; -LogIC(50) 7.03+/-0.22; n=9) and KCl (E(max) 74.14+/-5.61%; -LogIC(50) 2.12+/-0.07; n=10)-induced relaxations were attenuated (P0.0001) by removal of the endothelium (E(max) 8.21+/-5.39% and 11.56+/-8.49%, respectively; n=6 - 7). Indomethacin (10 microM) did not alter ACh-induced relaxation whereas L-NOARG (100 microM) reduced this response (E(max) 61.7+/-3.4%, P0.0001; n=6). The combination of ChTx (50 nM) and apamin (30 nM) attenuated the L-NOARG-insensitive component of ACh-induced relaxation (E(max): 15.2+/-10.5%, P0.002, n=6) although these arteries retained the ability to relax in response to 100 microM SIN-1 (E(max) 127.6+/-13.0%, n=3). Exposure to BaCl(2) (30 microM) and Ouabain (1 mM) did not attenuate the L-NOARG resistant component of ACh-mediated relaxation (E(max), 76.09+/-8.92, P=0.16; n=5). KCl-mediated relaxation was unaffected by L-NOARG+indomethacin (E(max); 68.1+/-5.6%, P=0.33; n=5) or the combination of L-NOARG/indomethacin/ChTx/apamin (E(max); 86.61+/-14.02%, P=0.35; n=6). In contrast, the combination of L-NOARG, indomethacin, ouabain and BaCl(2) abolished this response (E(max), 5.67+/-2.59%, P0.0001, n=6). The characteristics of KCl-mediated relaxation differed from those of the nitric oxide/prostaglandin-independent component of the response to ACh, and were endothelium-dependent, indicating that K(+) does not act as an EDHF in human subcutaneous resistance arteries.
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- 2001
21. Glucocorticoids play a key role in maturation and structural organisation of the developing zebrafish cardiovascular system
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Wilson, K. S., primary, Matrone, G., additional, Tucker, C. S., additional, Mullins, J. J., additional, Kenyon, C. J., additional, Hadoke, P. W. F., additional, and Denvir, M. A., additional
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- 2013
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22. Smooth Muscle Endothelin B Receptors Regulate Blood Pressure but Not Vascular Function or Neointimal Remodeling.
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Miller, Eileen, Czopek, Alicja, Duthie, Karolina M., Kirkby, Nicholas S., van de Putte, Elisabeth E. Fransen, Christen, Sibylle, Kimmitt, Robert A., Moorhouse, Rebecca, Castellan, Raphael F. P., Kotelevtsev, Yuri V., Kuc, Rhoda E., Davenport, Anthony P., Dhaun, Neeraj, Webb, David J., and Hadoke, Patrick W. F.
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The role of smooth muscle endothelinB (ETB) receptors in regulating vascular function, blood pressure (BP), and neointimal remodeling has not been established. Selective knockout mice were generated to address the hypothesis that loss of smooth muscle ETB receptors would reduce BP, alter vascular contractility, and inhibit neointimal remodeling. ETB receptors were selectively deleted from smooth muscle by crossing floxed ETB mice with those expressing cre-recombinase controlled by the transgelin promoter. Functional consequences of ETB deletion were assessed using myography. BP was measured by telemetry, and neointimal lesion formation induced by femoral artery injury. Lesion size and composition (day 28) were analyzed using optical projection tomography, histology, and immunohistochemistry. Selective deletion of ETB was confirmed by genotyping, autoradiography, polymerase chain reaction, and immunohistochemistry. ETB-mediated contraction was reduced in trachea, but abolished from mesenteric veins, of knockout mice. Induction of ETB-mediated contraction in mesenteric arteries was also abolished in these mice. Femoral artery function was unaltered, and baseline BP modestly elevated in smooth muscle ETB knockout compared with controls (+4.2±0.2 mm Hg; P<0.0001), but salt-induced and ETB blockade-mediated hypertension were unaltered. Circulating endothelin-1 was not altered in knockout mice. ETB-mediated contraction was not induced in femoral arteries by incubation in culture medium or lesion formation, and lesion size was not altered in smooth muscle ETB knockout mice. In the absence of other pathology, ETB receptors in vascular smooth muscle make a small but significant contribution to ETB-dependent regulation of BP. These ETB receptors have no effect on vascular contraction or neointimal remodeling. [ABSTRACT FROM AUTHOR]
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- 2017
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23. Inhibition of galectin-3 reduces atherosclerosis in apolipoprotein E-deficient mice
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MacKinnon, A. C., primary, Liu, X., additional, Hadoke, P. W., additional, Miller, M. R., additional, Newby, D. E., additional, and Sethi, T., additional
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- 2013
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24. MYELOID CELL 11β-HSD1 REGULATES THE INFLAMMATORY RESPONSE DURING MYOCARDIAL INFARCT HEALING AND PROTECTS THE HEART FROM DETRIMENTAL REMODELLING AFTER IRRADIATION AND BONE MARROW TRANSFER
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Mylonas, K J, primary, McGregor, K, additional, White, C, additional, Brooker, G, additional, Samuel, K, additional, Borthwick, G, additional, Hadoke, P W F, additional, Chapman, K C, additional, Walker, B R, additional, and Gray, G A, additional
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- 2012
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25. Non-endothelial cell endothelin-B receptors limit neointima formation following vascular injury
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Kirkby, N. S., primary, Duthie, K. M., additional, Miller, E., additional, Kotelevtsev, Y. V., additional, Bagnall, A. J., additional, Webb, D. J., additional, and Hadoke, P. W. F., additional
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- 2012
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26. Inhaled Nanoparticles Accumulate at Sites of Vascular Disease
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Miller, Mark R., Raftis, Jennifer B., Langrish, Jeremy P., McLean, Steven G., Samutrtai, Pawitrabhorn, Connell, Shea P., Wilson, Simon, Vesey, Alex T., Fokkens, Paul H. B., Boere, A. John F., Krystek, Petra, Campbell, Colin J., Hadoke, Patrick W. F., Donaldson, Ken, Cassee, Flemming R., Newby, David E., Duffin, Rodger, and Mills, Nicholas L.
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The development of engineered nanomaterials is growing exponentially, despite concerns over their potential similarities to environmental nanoparticles that are associated with significant cardiorespiratory morbidity and mortality. The mechanisms through which inhalation of nanoparticles could trigger acute cardiovascular events are emerging, but a fundamental unanswered question remains: Do inhaled nanoparticles translocate from the lung in man and directly contribute to the pathogenesis of cardiovascular disease? In complementary clinical and experimental studies, we used gold nanoparticles to evaluate particle translocation, permitting detection by high-resolution inductively coupled mass spectrometry and Raman microscopy. Healthy volunteers were exposed to nanoparticles by acute inhalation, followed by repeated sampling of blood and urine. Gold was detected in the blood and urine within 15 min to 24 h after exposure, and was still present 3 months after exposure. Levels were greater following inhalation of 5 nm (primary diameter) particles compared to 30 nm particles. Studies in mice demonstrated the accumulation in the blood and liver following pulmonary exposure to a broader size range of gold nanoparticles (2–200 nm primary diameter), with translocation markedly greater for particles <10 nm diameter. Gold nanoparticles preferentially accumulated in inflammation-rich vascular lesions of fat-fed apolipoproteinE-deficient mice. Furthermore, following inhalation, gold particles could be detected in surgical specimens of carotid artery disease from patients at risk of stroke. Translocation of inhaled nanoparticles into the systemic circulation and accumulation at sites of vascular inflammation provides a direct mechanism that can explain the link between environmental nanoparticles and cardiovascular disease and has major implications for risk management in the use of engineered nanomaterials.
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- 2017
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27. YIA 3 Effect of intracellular glucocorticoid metabolism on neointimal proliferation in a mouse model of wire angioplasty
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Iqbal, J., primary, Macdonald, L. J., additional, Yau, C. W., additional, Walker, B. R., additional, and Hadoke, P. W. F., additional
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- 2011
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28. Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation
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Mills, N. L., primary, Miller, M. R., additional, Lucking, A. J., additional, Beveridge, J., additional, Flint, L., additional, Boere, A. J. F., additional, Fokkens, P. H., additional, Boon, N. A., additional, Sandstrom, T., additional, Blomberg, A., additional, Duffin, R., additional, Donaldson, K., additional, Hadoke, P. W. F., additional, Cassee, F. R., additional, and Newby, D. E., additional
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- 2011
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29. YIA2 11 -HSD1 deficiency attenuates atherosclerosis in ApoE-/- mice: role of both glucocorticoid and non-glucocorticoid (oxysterol) factors
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Mitic, T., primary, Hadoke, P. W. F., additional, Chuaiphichai, S., additional, Man, T. Y., additional, Miller, E., additional, Andrew, R., additional, Walker, B. R., additional, Chapman, K. E., additional, and Seckl, J. R., additional
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- 2010
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30. BAS/BSCR27 Diesel exhaust particles promote atherosclerosis in apolipoprotein E-deficient mice
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Miller, M. R., primary, McLean, S. G., additional, Duffin, R., additional, Shaw, C. A., additional, Mills, N. L., additional, Donaldson, K., additional, Newby, D. E., additional, and Hadoke, P. W. F., additional
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- 2010
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31. BAS/BSCR13 Increased plasminogen activator inhibitor-1 may explain dexamethasone-induced thrombosis as site of intraluminal wire injury
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Low, L., primary, Seckl, J. R., additional, Walker, B. R., additional, and Hadoke, P. W. F., additional
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- 2010
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32. A Protocol for Improved Measurement of Arterial Flow Rate in Preclinical Ultrasound.
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Kenwright, D. A., Thomson, A. J. W., Hadoke, P. W. F., Anderson, T., Moran, C. M., Gray, G. A., and Hoskins, P. R.
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- 2015
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33. Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure
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Hadoke, P W F, primary, Lindsay, R S, additional, Seckl, J R, additional, Walker, B R, additional, and Kenyon, C J, additional
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- 2006
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34. Endothelium-derived hyperpolarizing factor and potassium use different mechanisms to induce relaxation of human subcutaneous resistance arteries
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McIntyre, C-A, primary, Buckley, C H, additional, Jones, G C, additional, Sandeep, T C, additional, Andrews, R C, additional, Elliott, A I, additional, Gray, G A, additional, Williams, B C, additional, McKnight, J A, additional, Walker, B R, additional, and Hadoke, P W F, additional
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- 2001
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35. Sertoli Cells Modulate Testicular Vascular Network Development, Structure, and Function to Influence Circulating Testosterone Concentrations in Adult Male Mice
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Rebourcet, Diane, Wu, Junxi, Cruickshanks, Lyndsey, Smith, Sarah E., Milne, Laura, Fernando, Anuruddika, Wallace, Robert J., Gray, Calum D., Hadoke, Patrick W. F., Mitchell, Rod T., O'Shaughnessy, Peter J., and Smith, Lee B.
- Abstract
The testicular vasculature forms a complex network, providing oxygenation, micronutrients, and waste clearance from the testis. The vasculature is also instrumental to testis function because it is both the route by which gonadotropins are delivered to the testis and by which T is transported away to target organs. Whether Sertoli cells play a role in regulating the testicular vasculature in postnatal life has never been unequivocally demonstrated. In this study we used models of acute Sertoli cell ablation and acute germ cell ablation to address whether Sertoli cells actively influence vascular structure and function in the adult testis. Our findings suggest that Sertoli cells play a key role in supporting the structure of the testicular vasculature. Ablating Sertoli cells (and germ cells) or germ cells alone results in a similar reduction in testis size, yet only the specific loss of Sertoli cells leads to a reduction in total intratesticular vascular volume, the number of vascular branches, and the numbers of small microvessels; loss of germ cells alone has no effect on the testicular vasculature. These perturbations to the testicular vasculature leads to a reduction in fluid exchange between the vasculature and testicular interstitium, which reduces gonadotropin-stimulated circulating T concentrations, indicative of reduced Leydig cell stimulation and/or reduced secretion of T into the vasculature. These findings describe a new paradigm by which the transport of hormones and other factors into and out of the testis may be influenced by Sertoli cells and highlights these cells as potential targets for enhancing this endocrine relationship.
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- 2016
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36. Role of the endothelium in modulating functional responses of isolated bovine anterior ciliary arteries to vasoconstrictor agonists
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Buckley, C. H, primary, Hadoke, P. W F, additional, and O'Brien, C. J, additional
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- 1998
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37. Preservation of vascular function in rat mesenteric resistance arteries following cold storage, studied by small vessel myography
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McIntyre, C. A., primary, Williams, B. C., additional, Lindsay, R. M., additional, McKnight, J. A., additional, and Hadoke, P. W. F., additional
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- 1998
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38. Effect of propranolol on vascular hyporesponsiveness in cirrhosis
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HADOKE, P. W. F., primary
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- 1997
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39. Use of isolated ocular arteries in vitro to define the pathology of vascular changes in glaucoma
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BUCKLEY, C. H, primary, HADOKE, P. W F, additional, and O'BRIEN, C. J, additional
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- 1997
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40. An improved ex vivo method of primary porcine hepatocyte isolation for use in bioartificial liver systems.
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Nelson, L J, Newsome, P N, Howie, A F, Hadoke, P W, Dabos, K J, Walker, S W, Hayes, P C, and Plevris, J N
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- 2000
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41. Platelet function in cirrhosis and the role of humoral factors.
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Younger, Hazel M., Hadoke, Patrick W.F., Dillon, John F., Hayes, Peter C., Younger, H M, Hadoke, P W, Dillon, J F, and Hayes, P C
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- 1997
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42. Adverse cardiovascular effects of air pollution
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Mills, Nicholas L, Donaldson, Ken, Hadoke, Paddy W, Boon, Nicholas A, MacNee, William, Cassee, Flemming R, Sandström, Thomas, Blomberg, Anders, and Newby, David E
- Abstract
Millset al. explore the preclinical and clinical evidence and examine the potential pathways through which air pollution—an important and modifiable determinant of cardiovascular disease—mediates adverse cardiovascular effects. Understanding the mediators and mechanisms will enable the development of strategies to reduce the impact of air pollution on cardiovascular disease.
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- 2009
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43. Acute Effects of Glucocorticoids on Endothelial Fibrinolytic and Vasodilator Function in Humans
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Dover, Anna R, Hadoke, Patrick W F, Walker, Brian R, and Newby, David E
- Abstract
Acute coronary events occur most commonly in the morning, when circadian variations dictate that endogenous fibrinolytic activity is low and cortisol levels are high. We hypothesized that glucocorticoids would impair the acute fibrinolytic capacity of the endothelium because chronic glucocorticoid excess is associated with a prothrombotic state and endothelial vasomotor dysfunction. Twelve healthy subjects attended on 3 occasions and received oral metyrapone followed by intravenous saline or low-dose or high-dose hydrocortisone. Forearm blood flow and fibrinolytic indices were measured using venous occlusion plethysmography during intrabrachial bradykinin, acetylcholine, and sodium nitroprusside infusion.
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- 2007
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44. Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure
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Hadoke, P W F, Lindsay, R S, Seckl, J R, Walker, B R, and Kenyon, C J
- Abstract
Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. The mechanisms underlying this programmed elevation of blood pressure have not been established. We hypothesised that prenatal glucocorticoid exposure may lead to vascular dysfunction in adulthood. Pregnant rats received dexamethasone (Dex) (100 μg/kg, s.c.) or vehicle (control) daily throughout pregnancy. Blood pressure was elevated (students t-test, unpaired; P< 0.05) in adult female offspring (aged 12–16 weeks) of Dex-treated mothers (148.0 ± 3.6 mmHg, n=10) compared with the control group (138.0 ± 2.5 mmHg, n=8). Vascular responsiveness in aortae and mesenteric arteries was differentially affected by prenatal Dex: aortae were less responsive to angiotensin II, whereas mesenteric arteries were more responsive to norepinephrine, vasopressin and potassium (mesenteric arteries respond poorly to angiotensin II in vitro). Acetylcholine-mediated, endothelium-dependent relaxation was similar in both groups. Prenatal exposure to Dex had no effect on blood pressure or aldosterone response to acute (15 min, i.v.) infusion of angiotensin II (75 ng/kg per min). In contrast, chronic (2-week, s.c.) infusion of angiotensin II (100 ng/kg per min) produced a greater elevation (P< 0.05) of blood pressure in Dex-treated rats (150.0 ± 3.6 mmHg) than in controls (135.3 ± 5.4 mmHg), and aldosterone levels were higher in Dex-treated animals. There was no angiotensin II-induced medial hypertrophy/hyperplasia in mesenteric arteries from Dex-treated rats. These results indicate that vascular function is altered in a region-specific manner in rats with glucocorticoid-programmed hypertension. Despite a striking increase in mesenteric artery contraction in Dex-treated rats, in vivostudies suggest that abnormalities of the renin-angiotensin-aldosterone system, rather than enhanced vascular contractility, may be responsible for the elevation of blood pressure in these animals.
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- 2005
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45. Selective enhancement of sensitivity to endothelin-1 despite normal endothelium-dependent relaxation in subcutaneous resistance arteries isolated from patients with Type I diabetes
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MCINTYRE, Carol-Ann, HADOKE, Patrick W. F., WILLIAMS, Brent C., LINDSAY, R. Mark, ELLIOTT, Andrew I., and MCKNIGHT, John A.
- Abstract
Type I diabetes mellitus is associated with abnormal vascular function, but few studies have documented its effects on human resistance arteries. This study aimed to determine whether endothelial cell and smooth muscle cell function was impaired in resistance arteries isolated from patients with this condition. Biopsies of subcutaneous gluteal fat were taken from 12 patients with Type I diabetes (age 32.3±1.9 years; duration of diabetes 13.9±2.5 years) and 12 matched controls (age 31.5±2.2 years). Levels of glycosylated haemoglobin were higher (P < 0.0001) in patients (9.38±0.35%) than in controls (5.48±0.11%), but most (11 out of 12) patients showed no evidence of microvascular disease. Small resistance arteries were isolated from the biopsies, and isometric responses to vasoconstrictors and vasodilators were measured in a small-vessel myograph. The magnitude and sensitivity of responses to noradrenaline and potassium were not different in diabetic patients compared with controls. In contrast, the sensitivity (pD2; negative logarithm of the concentration of the vasoconstrictor required to produce 50% of the maximum effect), but not the magnitude, of contraction in response to endothelin-1 in vessels from patients (8.87±0.12) was significantly (P = 0.02) greater than in those from controls (8.40±0.13). Endothelium-dependent (acetylcholine, bradykinin, A23187) and -independent (3´-morpholinosydnonimine) relaxation responses were unaltered in patients with Type I diabetes. These results suggest a selective alteration in receptor activity in the endothelium, and contrast strikingly with the considerable evidence of impaired endothelium-dependent relaxation in Type I diabetes. The present study indicates, therefore, that endothelial cell function is largely maintained in resistance arteries from patients with well controlled Type I diabetes. The increased response to endothelin-1 supports the possibility that more significant abnormalities would be evident in patients with severe microvascular complications.
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- 2001
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46. Cirrhosis of the liver and receptor-mediated function in vascular smooth muscle
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Hadoke, P. W.
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- 2001
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47. Functional heterogeneity of large and small resistance arteries isolated from biopsies of subcutaneous fat
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Hadoke, P. W., McIntyre, C. A., Gray, G. A., and Buckley, C. H.
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- 2000
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48. 35th Annual Meeting of the European Association for the Study of Diabetes
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Juhl, C., Pørksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th., Müller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Björn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H.-M., Oksanen, L., Tuomainen, T.-P., Kontula, K., Salonen, J. T., Dekker, J. M., de Boks, P., de Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D’Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., MacAlpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M., Kozáková, H., Kaas, A., Kofronová, O., Tlaskalová-Hogenová, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sørensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Haskó, G., Szabó, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Van Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H.-H., Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabák, Á. Gy., Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Cantón, A., Burgos, R., Hernández, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simó, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., McDermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y.-S., Sternesjö, J., Sandler, S., Chen, M.-C., Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Bréant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., van der Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, De Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. I., Hamilton-Wessler, M., Markussen, J., Bergman, R. N., Melki, V., Hanaire-Broutin, H., Bessières-Lacombe, S., Tauber, J.-P., Home, P. D., Lindholm, A., Riis, A., Rosenstock, J., Schwartz, S., Clark, C., Edwards, M., Donley, D., Swift, P., Mortensen, H. B., Lynggaard, H., Hougaard, P., Cull, C. A., Neil, H. A. W., Frighi, V., Manley, S. E., Holman, R. R., Turner, R. C., Steiner, G., Davis, W. A., Weeraratna, T., Bruce, D. G., Davis, T. M. E., Vergès, B., Duvillard, L., Pont, F., Florentin, E., Gambert, Ph., Benko, B., Ljubić, S., Turk, Z., Granić, M., März, W., Wollschläger, H., Klein, G., Neiss, A., Wehling, M., Huxtable, S. J., Saker, P. J., Walker, M., Frayling, T. M., Levy, J. C., O’Rahilly, S., Hattersley, A. T., McCarthy, M. I., Orecchio, A., Giacchini, A., Dominici, R., Canettieri, G., Trinti, B., Zani, M., Andreoli, M., Sciacchitano, S., de Silva, A. M., Whitecross, K., Pasco, J., Kotowicz, M., Nicholson, G., Zimmet, P., Boyko, E. J., Collier, G. R., Frittitta, L., Pizzuti, A., Argiolas, A., Graci, S., Goldfine, I. D., Bozzali, M., Ercolino, T., Costanzo, B., Iacoviello, L., Tassi, V., Trischitta, V., Wauters, M., Rankinen, T., Mertens, I., Chagnon, M., Bouchard, C., Van Gaal, L., Sivenius, K., Valve, R., Hakkarainen, V., Niskanen, L., Laakso, M., Uusitupa, M., Beridze, N., Japaridze, M., Kurashvili, R., Dundua, M., Kebuladze, G., Kazakhashvili, N., Offley-Shore, B., Thomas, B., Ghebremeskel, K., Crawford, M., Lowy, C., Eriksson, Ulf J., Martin Simán, C., Wisse, Bert, Gittenberger-de Groot, Adriana C., Wentzel, P., Eriksson, U. J., Wender-Ożegowska, E., Drews, K., Biczysko, R., Bronisz, A., Rość, D., Graczykowska-Koczorowska, A., Kotschy, M., Sokup, A., Kohnert, K. D., Besch, W., Strese, J., Frick, U., Zander, E., Kemer, W., Škrha, J., Kvasnička, J., Kalvodová, B., Hilgertová, J., Schatteman, K., Goossens, F., Scharpé, S., De Leeuw, I., Hendriks, D., Legakis, I. N., Panayiotou, D., Mountokalakis, Th. D., Enderle, M. D., Beckmann, P., Balletshofer, B., Rittig, K., Maerker, E., Volk, A., Meisner, C., Jacob, S., Matthaei, S., Häring, H. U., Rett, K., Ueda, K., Nakagawa, T., Shimajiri, Y., Kokawa, M., Matsumoto, E., Sasaki, H., Sanke, T., Nanjo, K., McKinnon, Caroline M., Macfarlane, Wendy M., Docherty, Kevin, Furukawa, N., Shirotani, T., Kishikawa, H., Kaneko, K., Araki, E., Shichiri, M., Prentki, M., Roduit, R., Susini, S., Buteau, J., Ejrnæs, A. M., Andersen, N. Aa., Osterhoff, M., Möhlig, M., Ortmann, J., Bikashaghi, F., Mayer, C., Bikashagi, F., Ackermans, M. T., Pereira Arias, A. M., Bisschop, P. H. L. T., Endert, E., Sauerwein, H. P., Romijn, J. A., Gastaldelli, A., Baldi, S., Pettiti, M., Natali, A., Frascerra, S., Camastra, S., Toschi, E., Ferrannini, E., Stingl, H., Krssak, M., Bischof, M. G., Krebs, M., Fürnsinn, C., Nowotny, P., Waldhäusl, W., Roden, M., Neeft, M., Meijer, A. J., Båvenholm, P., Pigon, J., Efendic, S., Kästenbauer, T., Sauseng, S., Sokol, G., Auinger, M., Irsigler, K., Abbott, C. A., Carrington, A. L., Faragher, B., Kulkarni, J., Van Ross, E. R. E., Boulton, A. J. M., Armstrong, D. G., Hadi, S., Nguyen, H. C., Harkless, L. B., Jirkovská, A., Kasalicky, P., Hosová, J., Skibova, J., Uccioli, L., Caselli, A., Giacomozzi, C., Macellari, V., Giurato, L., Lardieri, L., Menzinger, G., Pham, H. T., Rosenblum, B. I., Lyons, T. E., Giurini, J. M., Smakowski, P., Chrzan, J. S., Habershaw, G. M., Veves, A., Foster, A. M., Bates, M., Doxford, M., Edmonds, M. E., Kecha, O., Winkler, R., Martens, H., Collette, J., Lefèbvre, P. J., Greiner, D., Geenen, V., Atlan-Gepner, C., Naspetti, M., Valéro, R., Barad, M., Lepault, F., Vialettes, B., Naquet, P., de Galan, B., Netea, M. G., Hancu, N., Smits, P., Van der Meer, J. W. M., Osterbye, T., Jørgensen, K. H., Tranum-Jensen, J., Fredman, P., Høy, M., Bokvist, K., Olsen, H. L., Horn, T., Gromada, J., Laub, R., Lohmann, T., Hahn, H. J., Adler, T., Emmrich, F., Rabuazzo, A. M., Lupi, R., Dotta, F., Patanè, G., Marselli, L., Realacci, M., Piro, S., Del Guerra, S., Santangelo, C., Navalesi, R., Purrello, F., Marchetti, P., de Vos, P., Visser, L., de Haan, B. J., Klok, P., van Schilfgaarde, R., Poppema, S., Juang, J.-H., Kuo, C.-H., Hsu, B. R.-S., Nacher, V., Pérez, M., Biarnés, M., Raurell, M., Soler, J., Montanya, E., Ritzel, R., Maubach, J., Büsing, M., Becker, T., Klempnauer, J., Hücking, K., Schmiegel, W. H., Nauck, M. A., Bouček, P., Saudek, F., Adamec, M., Kožitarová, R., Jedináková, T., Vlasáková, Z., Skibová, J., Bartoš, V., Maffi, P., Bertuzzi, F., Aldrighetti, L., Taglietti, M. V., Castelnuovo, A., Pozza, G., Di Carlo, V., Secchi, A., Renier, G., Mamputu, J.-C., Gillespie, J. S., McMaster, D., Mercer, C., Trimble, E. R., Lecomte, M., Véricel, E., Paget, C., Ruggiero, D., Lagarde, M., Wiernsperger, N., Pricci, F., Leto, G., Amadio, L., Cordone, S., Iacobini, C., Catalano, S., Violi, F., Rotella, C. M., Pugliese, G., Zicari, A., Gradini, R., Sale, P., Pala, L., Cresci, B., Giannini, S., Manuelli, C., Dahlfors, G., Arnqvist, H. J., Gonelle-Gispert, C., Halnan, P. A., Sadoul, K., Wolter, S., Lang, J., Niwa, T., Yu, W., Hidaka, H., Senda, T., Niki, I., Fukasawa, T., Renstrom, E., Barg, S., Seward, E., Rorsman, P., Rutter, G. A., Molinete, M., Lilla, V., Ravazzola, M., Halban, P. A., Efanov, A. M., Bertorello, A. M., Zaitsev, S. V., Zwiller, J., Berggren, P.-O., MŞengül, A., Salman, F., Sargrn, M., Özer, E., Karşidaǧ, K., Salman, S., Gedik, S., Satman, İ., Dinççaǧ, N., Yılmaz, M. T., Lloyd, A., Hopkinson, P. K., Testa, M. A., Blonde, L., Turner, R. R., Hayes, J., Simonson, D. C., van der Ven, N. C. W., Lubach, C. H. C., Snoek, F. J., Mollema, E. D., van der Ploeg, H. M., Danne, T., Hoey, H., McGee, H., Fitzgerald, H., Lernmark, B., Thernlund, G., Fredin, K., Hägglöf, B., Lugari, R., Dell’Anna, C., Ugolotti, D., Dei Cas, A., Barilli, A. L., Sard, L., Marani, B., Iotti, M., Zandomeneghi, R., Gnudi, A., Kjems, L. L., Volund, Aa., Toft-Nielsen, M., Damholt, M. B., Hilsted, L., Hughes, T. E., Krarup, T., Holst, J. J., Young, A., Gottlieb, A., Fineman, M., Kolterman, O., Cancelas, J., García-Martínez, J. A., Villanueva-Peñacarrillo, M. L., Valverde, I., Malaisse, W. J., Filipsson, K., Ahrén, B., Balkan, B., Kwasnik, L., Battle, B., Li, X., Egan, J. M., Clocquet, A. R., Elahi, D., Petrella, E., Pricket, K., Petersen, K. F., Sullivan, J. T., Amatruda, J. M., Livingston, J. N., Shulman, G. I., Freyse, E.-J., Knospe, S., Glund, K., Demuth, H.-U., Walker, D., Malik, R. A., Reljanovic, M., Barada, A., Milicevic, Z., Tack, Cees J., Goldstein, David S., Van Huysen, C., Stevens, M. J., Cao, X., Sundkvist, G., Dahlin, L.-B., Eriksson, K.-F., Rosén, I., Lattimer, S. A., Sima, A. A. F., Sullivan, K., Shaw, J. E., de Courten, M. P., Zimmet, P. Z., Gourdy, P., Ruidavets, J. B., Arveiler, D., Amouyel, Ph., Bingham, A., Tauber, J. P., Lam, K. S. L., Wat, N. M. S., Lam, T. H., Janus, E. D., de Pablos, P., Rodriguez, F., Martínez, J., Sánchez, V., Santana, C., García, I., Macías, A., Levin, K., Hother-Nielsen, O., Henriksen, J. E., Beck-Nielsen, H., Brechtel, K., Machann, J., Koch, M., Nielsen, M., Löblein, K., Becker, R., Denignger, M., Renn, W., Machicao, F., Claussen, C. D., Schick, F., Diraison, F., Moulin, P., Beylot, M., Thams, P., Capito, K., Eliasson, Lena, Barg, Sebastian, Göpel, Sven, Kanno, Takahiro, Renström, Erik, Meda, P., Charollais, A., Gjnovci, A., Calabrese, A., Wonkam, A., Caton, D., Wisznievski, L., Serre, V., Cogne, F., Bauquis, J., Bosco, D., Huarte, J., Herrera, P., Gotfredsen, C. F., Vessby, B., Manuel y Keenoy, B., Engelen, W., Vertommen, J., Schrans, S., Louheranta, A., Lindström, J., Tuomilehto, J., Segal, K. R., Heymsfield, S., Hauptman, J., Boldrin, M., Lucas, C., Pandolfi, A., Cetrullo, D., Polishchuck, R., Alberta, M., Pellegrini, G., Calafiore, A., Vitacolonna, E., Capani, F., Consoli, A., Halleux, C. M., Gillot, E. F., Brichard, S. M., Van der Planken, M., Corthouts, B., Peiffer, F., Scholten, D., Walke, M., Assert, R., Pirags, V., Pedula, K. L., Hillier, T. A., Brown, J. B., Santini, S. A., Marra, G., Cotroneo, P., Manto, A., Di Leo, M. A. S., Di Gregorio, S., Tordi, A., Pitocco, D., Ruotolo, V., Ghirlanda, G., Temelkova-Kurktschiev, T., Schaper, F., Koehler, C., Henkel, E., Hanefeld, M., Mancini, L., Citterio, F., Cotroneo, A., Ceroone, S., Castagneto, M., Rajbhandari, S. M., Dent, M. T., Plater, M. E., Harris, N. D., Tesfaye, S., Ward, J. D., Dupuy, O., Mayaudon, H., Lecoules, S., Bauduceau, B., Palou, M., Farret, O., Molinié, C., Antonelli-Incalzi, R., Fuso, L., Giordano, A., Calcagni, M. L., Todaro, L., Basso, S., Tramaglino, L. M., Troncone, L., Pistelli, R., Guillot, R., Bringuier, A., Porokhov, B., Guillausseau, P. J., Feldmann, G., Zivanic, S., Cizmic, M., Dragojevic, R., Vanovic, M., Borghouts, L. B., van Kranenburg, G. P. J., Schaart, G., Keizer, H. A., Niess, A. M., Dickuth, H. H., Lutz, O., Barbe, P., Calazel-Fournier, C., Hernandez, G., Saint-Martin, F., Galitzky, J., Gonçalves, A. A., da Silva, E. C., Brito, I. J. L., da Silva, C. A., Lawrence, N. J., Kousta, E., Mulnier, H., Penny, A., Millauer, B., Johnston, D. G., Robinson, S., Perriello, G., Pimenta, W., Pampanelli, S., Lucidi, P., Lepore, M., Porcellati, F., Cordoni, M. C., De Feo, P., Bolli, G. B., Sjöstrand, M., Holmäng, A., Lönnroth, P., Hauer, B., Grauer, P., Artzner, S., Lang, R., Stumvoll, M., Monti, L. D., Piatti, P. M., Gemone, F., Valsecchi, G., Magni, M., Barbieri, E., Setola, E., Sandoli, E. P., Galli-Kienle, M., Pontiroli, A. E., Nichols, Gregory A., Brown, Jonathan B., Salzsieder, E., Boltz, H., Ramirez, J. C., Rutscher, A., Fischer, U., Koenig, Ch., Friske, M., Schramm, W., Landgraf, R., Bachmann, W., Bangemann, M., Groeneveld, G., Edvell, Anders, Lindström, Per, Tsiotra, P., Koukourava, A., Raptis, S. A., Tsigos, C., Boutou, E., Triandaffilopoulou, A., Egido, E. M., Rodríguez-Gallardo, J., Gutiérrez, E., García, P., Silvestre, R. A., Marco, J., Khan, Akhtar, Ling, Zong-Chao, Ahren, Bo, Efendic, Suad, Bünting, C., Du, X., Zhi Sui, G., Rösen, P., Koschinsky, T., Kearney, T. M., Sharp, P. S., Lapolla, A., Fedele, D., Martano, L., Garbeglio, M., Seraglia, R., Favretto, D., Traldi, P., Meerwaldt, R., Smit, A. J., Links, Th. P., v. Roon, A. M., Graaf, R., Gans, R. O. B., Deynelİ, O., Ersöz, H. Ö., Gogas, D., Fak, A. 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- Published
- 1999
- Full Text
- View/download PDF
49. Contractile response of isolated human hepatic arteries to α-adrenoceptor agonists is not impaired in patients with cirrhosis
- Author
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HADOKE, Patrick W. F., DILLON, John F., JOHN, Timothy G., WALKER, Simon W., HAYES, Peter C., and WILLIAMS, Brent C.
- Abstract
1.Impaired vasoconstriction in animals with cirrhosis is maintained in isolated vessels in vitro, indicating an intrinsic alteration in function or structure of the cells in the vascular wall. This may be due to receptor down-regulation, a defect in post-receptor signal transduction or overproduction of vasodilator compounds. This investigation examined the role of these mechanisms in modulating α-adrenoceptor-mediated contraction in hepatic arteries from patients with advanced cirrhosis. 2.Hepatic arteries were obtained from subjects with and without cirrhosis for functional investigation in vitro. Endothelial cell function was assessed using endothelium-dependent (acetylcholine) and independent (3′-morpholinosydnonimine) vasodilators. α-Adrenoceptor-mediated contraction was assessed by constructing cumulative concentration–response curves to the α1-selective agonist phenylephrine, the non-selective adrenoceptor agonist noradrenaline and the receptor-independent vasoconstrictor potassium chloride. 3.None of the vessels used in this study had an intact endothelium but endothelium-independent relaxation was not different in arteries from subject with (79.5±10.16%; n = 23) and without (84.45±18%; n = 20) cirrhosis. Phenylephrine, noradrenaline and potassium chloride produced contractions that were of similar size (P> 0.05) in arteries from subjects with (10.10±0.97 ;g, 8.85±1.03 ;g and 8.56±0.65 ;g respectively) and without (10.42±1.23 ;g, 9.58±1.39 ;g and 8.62±0.98 ;g respectively) cirrhosis. The sensitivities (pD2) of the responses to these agonists were also similar (P< 0.05) in arteries from patients with cirrhosis (5.45±0.10, 5.60±0.12 and 1.57±0.03 respectively) and those from non-cirrhotic donors (5.58±0.11, 5.67±0.11 and 1.54±0.05 respectively). 4.Contraction of the denuded hepatic artery was unaffected by cirrhosis indicating that vascular abnormalities in this condition in man are not due to an intrinsic alteration of smooth muscle cell function in hepatic conduit arteries.
- Published
- 1998
- Full Text
- View/download PDF
50. In Vitro Evidence for Vascular Hyporesponsiveness in Clinical and Experimental Cirrhosis
- Author
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Hadoke, P. W. F. and Hayes, P. C.
- Published
- 1997
- Full Text
- View/download PDF
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