18 results on '"Dong, Yi-Fei"'
Search Results
2. Plasma Homocysteine Levels Are Associated With Circadian Blood Pressure Variation in Chinese Hypertensive Adults.
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Dong YF, Zhan BM, Hao QY, Ruan ZH, Xu ZX, Deng M, Chen DW, Zou YQ, Chen J, Li P, and Cheng XS
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- Adult, Aged, Asian People, Blood Pressure Monitoring, Ambulatory, Female, Genotype, Humans, Hypertension genetics, Hypertension physiopathology, Male, Methylenetetrahydrofolate Reductase (NADPH2) genetics, Middle Aged, Polymorphism, Genetic, Blood Pressure, Circadian Rhythm, Homocysteine blood, Hypertension blood
- Abstract
Background: Homocysteine-lowering intervention with folate was recently shown to be able to increase day-night difference of blood pressure (BP) in humans indicating a potential relationship between homocysteine and circadian BP variation. We thus sought to investigate the association between plasma total homocysteine level (tHcy) and circadian BP variation in hypertensive adults., Methods: We enrolled 244 eligible dipping and 249 nondipping BP status adults from 560 adults who were randomly sampled from 5,233 Chinese hypertensive adults who received ambulatory BP monitoring (ABPM). We further enrolled 390 adults with CC/CT genotypes of the methylenetetrahydrofolate reductase (MTHFR) and 79 TT genotype who received ABPM at the same time from 1858 hypertensive adults with MTHFR polymorphisms detection., Results: Plasma tHcy in nondippers was significantly higher than dippers (P < 0.001). Simple linear analysis revealed that tHcy significantly correlated with nocturnal systolic BP fall (r = -0.145, P = 0.001) and diastolic BP fall (r = -0.141, P = 0.002). Multivariate logistic regression analysis further identified tHcy as an independent factor correlated with the presence of nondipping BP status in hypertensive adults (odds ratio: 1.873, 95% confidence interval: 1.171-2.996, P = 0.009). The percentage of dipping BP status was 19.49% or 8.86% and the percentage of nondipping BP status was 80.51% or 91.14% in CC/CT or TT genotypes, respectively. The above different between CC/CT and TT genotypes was significant (P = 0.024)., Conclusions: These results indicated that high homocysteine levels associate with disturbed circadian BP variation in Chinese hypertensive adults., (© American Journal of Hypertension, Ltd 2017. All rights reserved. For Permissions, please email: journals.permissions@oup.com)
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- 2017
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3. Independent association between age and circadian systolic blood pressure patterns in adults with hypertension.
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Deng M, Chen DW, Dong YF, Lu P, Zhan BM, Xu JQ, Ji XX, Li P, and Cheng XS
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- Adult, Age Factors, Aged, Antihypertensive Agents therapeutic use, Blood Pressure drug effects, Blood Pressure Monitoring, Ambulatory methods, Body Mass Index, Comorbidity, Female, Heart Rate physiology, Humans, Hypertension drug therapy, Hypotension physiopathology, Male, Middle Aged, Systole drug effects, Blood Pressure physiology, Circadian Rhythm physiology, Hypertension physiopathology, Systole physiology
- Abstract
Previous studies indicate a preliminary association between age and circadian blood pressure (BP) variation. This association would be affected by confounding factors in real-world populations. The authors investigated whether this is a convincingly independent association in a real-world population of adults with hypertension. Clinical data and findings of 24-hour ambulatory BP monitoring were obtained from 297 consecutive adults with hypertension (60.19±0.77 years). BP dipping patterns were categorized based on the percentage of nocturnal BP drop. Multivariate linear regression analysis identified an independent correlation between age and percentage of nocturnal systolic BPdrop (β=-7.296; 95% CI, -10.430 to -4.162 [P<.001]). Reverse dippers were the oldest and extreme dippers were the youngest. A significant age difference was noted among patients grouped into four BP dipping patterns with and without adjustments for sex, body mass index, drugs, diabetes mellitus, smoking, 24-hour mean heart rate, and 24-hour mean systolic and diastolic BP., (©2017 Wiley Periodicals, Inc.)
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- 2017
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4. Association of Endothelial and Mild Renal Dysfunction With the Severity of Left Ventricular Hypertrophy in Hypertensive Patients.
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Cao C, Hu JX, Dong YF, Zhan R, Li P, Su H, Peng Q, Wu T, Huang X, Sun WH, Wu QH, and Cheng XS
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- Aged, Cross-Sectional Studies, Female, Glomerular Filtration Rate, Humans, Hyperemia physiopathology, Hypertension diagnosis, Hypertension physiopathology, Hypertrophy, Left Ventricular diagnosis, Hypertrophy, Left Ventricular physiopathology, Kidney Diseases diagnosis, Kidney Diseases physiopathology, Linear Models, Logistic Models, Male, Middle Aged, Multivariate Analysis, Odds Ratio, Risk Factors, Vascular Stiffness, Blood Pressure, Endothelium, Vascular physiopathology, Hypertension complications, Hypertrophy, Left Ventricular etiology, Kidney physiopathology, Kidney Diseases etiology, Vascular Remodeling
- Abstract
Background: The association between impaired renal function and increase left ventricular mass was shown to be related to increase in arterial stiffness, which indicates that vascular homeostasis and remodeling may impact the left ventricular hypertrophy (LVH) in patients with renal dysfunction., Methods: We measured the peripheral arterial reactive hyperemia index (RHI) and estimated glomerular filtration rate (eGFR) in 317 hypertensive patients comprising 115 normal RHI (RHI > 1.67) and normal eGFR (eGFR ≥ 90ml/min per 1.73 m(2)), 136 low RHI (RHI ≤ 1.67), 27 low eGFR (60 ≤ eGFR < 90ml/min per 1.73 m(2)) and 39 low RHI combined with low eGFR., Results: Multivariate logistic regression analysis identified lg RHI (odds ratio (OR): 0.001, 95% confidence interval (CI): 10(-6) to 0.426, P = 0.024) and lg eGFR (OR: 0.009, 95% CI: 10(-4) to 0.414, P = 0.016) as independent factors correlated with LVH respectively in hypertensive patients. Compared with normal RHI and eGFR patients, the extent of LVH in patients with either low RHI (OR: 1.224 95% CI: 0.451 to 3.327, P = 0.691) or low eGFR (OR: 0.593 95% CI: 0.070 to 5.037, P = 0.632) did not significantly increase, while it increased significantly in patients with low RHI combined with low eGFR (OR: 4.629 95% CI: 1.592 to 13.458, P = 0.005)., Conclusions: The concurrence of endothelial and mild renal dysfunction was significantly associated with the severity of LVH in hypertensive patients., (© American Journal of Hypertension, Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)
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- 2016
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5. Novel mechanism of angiotensin II-induced cardiac injury in hypertensive rats: the critical role of ASK1 and VEGF.
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Nako H, Kataoka K, Koibuchi N, Dong YF, Toyama K, Yamamoto E, Yasuda O, Ichijo H, Ogawa H, and Kim-Mitsuyama S
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- Animals, Antihypertensive Agents pharmacology, Apoptosis drug effects, Biphenyl Compounds pharmacology, Blood Pressure physiology, Blotting, Western, Capillaries drug effects, Cells, Cultured, Cyclic N-Oxides pharmacology, Endothelial Cells drug effects, Heart Diseases diagnostic imaging, Heart Diseases pathology, Hydralazine pharmacology, Hypertension complications, Hypertension diagnostic imaging, Hypertrophy, Left Ventricular pathology, Immunohistochemistry, Irbesartan, Myocardial Ischemia physiopathology, Oxidative Stress drug effects, Rats, Rats, Inbred Dahl, Reactive Oxygen Species metabolism, Real-Time Polymerase Chain Reaction, Spin Labels, Superoxides metabolism, Tetrazoles pharmacology, Ultrasonography, Angiotensin II toxicity, Heart Diseases chemically induced, Hypertension physiopathology, MAP Kinase Kinase Kinase 5 physiology, Vascular Endothelial Growth Factor A physiology
- Abstract
This study was undertaken to elucidate a novel mechanism underlying angiotensin II-induced cardiac injury, focusing on the role of oxidative stress and myocardial capillary density. Salt-loaded Dahl salt-sensitive hypertensive rats (DS rats), a useful model for hypertensive cardiac remodeling or heart failure, were orally given irbesartan (an AT1 receptor blocker), tempol (a superoxide dismutase mimetic) or hydralazine (a vasodilator). Irbesartan significantly ameliorated left ventricular ischemia and prevented the development of cardiac hypertrophy and fibrosis in DS rats. The benefits were associated with the attenuation of oxidative stress, normalization of myocardial capillary density and inhibition of capillary endothelial apoptosis. Moreover, DS rats with significant cardiac hypertrophy and fibrosis displayed decreased myocardial vascular endothelial growth factor (VEGF) expression and increased cardiac apoptosis signal-regulating kinase 1 (ASK1) activation. Treatment with irbesartan significantly reversed these phenotypes. Tempol treatment of DS rats mimicked all the above-mentioned effects of irbesartan, indicating the critical role of oxidative stress in cardiac injury. We also investigated the role of VEGF and ASK1 in oxidative stress-induced endothelial apoptosis by using cultured endothelial cells from wild-type and ASK1-deficient mice. Oxidative stress-induced ASK1 activation led to endothelial apoptosis, and VEGF treatment prevented oxidative stress-induced endothelial apoptosis by inhibiting ASK1 activation. We obtained the first evidence that oxidative stress-induced cardiac VEGF repression and ASK1 activation caused the enhancement of endothelial apoptosis and contributed to a decrease in myocardial capillary density. These effects resulted in angiotensin II-induced progression of cardiac injury.
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- 2012
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6. Calcium channel blockers, more than diuretics, enhance vascular protective effects of angiotensin receptor blockers in salt-loaded hypertensive rats.
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Yamamoto E, Kataoka K, Dong YF, Koibuchi N, Toyama K, Sueta D, Katayama T, Yasuda O, Ogawa H, and Kim-Mitsuyama S
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- Animals, Diuretics pharmacology, Oxidative Stress, Rats, Angiotensin Receptor Antagonists pharmacology, Calcium Channel Blockers pharmacology, Hypertension prevention & control
- Abstract
The combination therapy of an angiotensin receptor blocker (ARB) with a calcium channel blocker (CCB) or with a diuretic is favorably recommended for the treatment of hypertension. However, the difference between these two combination therapies is unclear. The present work was undertaken to examine the possible difference between the two combination therapies in vascular protection. Salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP) were divided into 6 groups, and they were orally administered (1) vehicle, (2) olmesartan, an ARB, (3) azelnidipine, a CCB, (4) hydrochlorothiazide, a diuretic, (5) olmesartan combined with azelnidipine, or (6) olmesartan combined with hydrochlorothiazide. Olmesartan combined with either azelnidipine or hydrochlorothiazide ameliorated vascular endothelial dysfunction and remodeling in SHRSP more than did monotherapy with either agent. However, despite a comparable blood pressure lowering effect between the two treatments, azelnidipine enhanced the amelioration of vascular endothelial dysfunction and remodeling by olmesartan to a greater extent than did hydrochlorothiazide in salt-loaded SHRSP. The increased enhancement by azelnidipine of olmesartan-induced vascular protection than by hydrochlorothiazide was associated with a greater amelioration of vascular nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation, superoxide, mitogen-activated protein kinase activation, and with a greater activation of the Akt/endothelial nitric oxide synthase (eNOS) pathway. These results provided the first evidence that a CCB potentiates the vascular protective effects of an ARB in salt-sensitive hypertension, compared with a diuretic, and provided a novel rationale explaining the benefit of the combination therapy with an ARB and a CCB.
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- 2012
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7. Beneficial effects of combination of valsartan and amlodipine on salt-induced brain injury in hypertensive rats.
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Dong YF, Kataoka K, Tokutomi Y, Nako H, Nakamura T, Toyama K, Sueta D, Koibuchi N, Yamamoto E, Ogawa H, and Kim-Mitsuyama S
- Subjects
- Amlodipine pharmacology, Angiotensin II Type 1 Receptor Blockers pharmacology, Animals, Blood Pressure drug effects, Brain metabolism, Brain pathology, Calcium Channel Blockers pharmacology, Calcium Channels drug effects, Carotid Arteries anatomy & histology, Carotid Arteries drug effects, Drug Therapy, Combination, Endothelial Cells drug effects, Endothelial Cells pathology, Hypertension pathology, Hypoxia-Ischemia, Brain chemically induced, Male, Nitric Oxide analysis, Nitric Oxide biosynthesis, Nitric Oxide Synthase Type III analysis, Nitric Oxide Synthase Type III biosynthesis, Random Allocation, Rats, Rats, Inbred SHR, Receptor, Angiotensin, Type 1 drug effects, Sodium Chloride, Dietary toxicity, Tetrazoles pharmacology, Tyrosine analogs & derivatives, Tyrosine analysis, Tyrosine biosynthesis, Valine pharmacology, Valine therapeutic use, Valsartan, Amlodipine therapeutic use, Angiotensin II Type 1 Receptor Blockers therapeutic use, Brain physiopathology, Calcium Channel Blockers therapeutic use, Hypertension drug therapy, Tetrazoles therapeutic use, Valine analogs & derivatives
- Abstract
The optimum antihypertensive treatment for prevention of hypertensive stroke has yet to be elucidated. This study was undertaken to examine the benefit of a combination of valsartan, an angiotensin II type 1 (AT1) receptor blocker, and amlodipine, a calcium channel blocker, in prevention of high-salt-induced brain injury in hypertensive rats. High-salt-loaded stroke-prone spontaneously hypertensive rats (SHRSPs) were given 1) vehicle, 2) valsartan (2 mg/kg/day), 3) amlodipine (2 mg/kg/day), or 4) a combination of valsartan and amlodipine for 4 weeks. The effects on brain injury were compared between all groups. High-salt loading in SHRSPs caused the reduction of cerebral blood flow (CBF), cerebral hypoxia, white matter lesions, glial activation, AT1 receptor up-regulation, endothelial nitric-oxide synthase (eNOS) uncoupling, inducible nitric-oxide synthase induction, and nitroxidative stress. Valsartan, independently of blood pressure, enhanced the protective effects of amlodipine against brain injury, white matter lesions, and glial activation in salt-loaded SHRSPs. These beneficial effects of valsartan added to amlodipine were associated with an additive improvement in CBF and brain hypoxia because of an additive improvement in cerebral arteriolar remodeling and vascular endothelial dysfunction. Furthermore, valsartan added to amlodipine enhanced the attenuation of cerebral nitroxidative stress through an additive suppression of eNOS uncoupling. Valsartan, independently of blood pressure, augmented the protective effects of amlodipine against brain injury in salt-loaded hypertensive rats through an improvement in brain circulation attributed to nitroxidative stress. Our results suggest that the combination of valsartan and amlodipine may be a promising strategy for the prevention of salt-related brain injury in hypertensive patients.
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- 2011
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8. Eplerenone potentiates protective effects of amlodipine against cardiovascular injury in salt-sensitive hypertensive rats.
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Nakamura T, Fukuda M, Kataoka K, Nako H, Tokutomi Y, Dong YF, Yamamoto E, Yasuda O, Ogawa H, and Kim-Mitsuyama S
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- Aldosterone blood, Amlodipine administration & dosage, Animals, Antihypertensive Agents administration & dosage, Blood Pressure drug effects, Carotid Arteries drug effects, Carotid Arteries metabolism, Drug Therapy, Combination, Endothelium, Vascular drug effects, Endothelium, Vascular physiopathology, Eplerenone, Hypertension physiopathology, Male, Mineralocorticoid Receptor Antagonists administration & dosage, Myocardium metabolism, Nitric Oxide Synthase Type III metabolism, Oxidative Stress drug effects, Oxidative Stress physiology, Proto-Oncogene Proteins c-akt metabolism, Rats, Rats, Inbred Dahl, Receptor, Angiotensin, Type 1 metabolism, Sodium Chloride, Dietary pharmacology, Spironolactone administration & dosage, Spironolactone therapeutic use, Superoxides metabolism, Treatment Outcome, Amlodipine therapeutic use, Antihypertensive Agents therapeutic use, Heart drug effects, Hypertension drug therapy, Mineralocorticoid Receptor Antagonists therapeutic use, Spironolactone analogs & derivatives
- Abstract
The clinical value of the combination of amlodipine and eplerenone is unclear. This study was undertaken to test whether eplerenone potentiates the protective effects of amlodipine against hypertensive cardiovascular injury. Salt-loaded Dahl salt-sensitive hypertensive rats (DS rats) were given (1) vehicle, (2) an antihypertensive dose of amlodipine, (3) a non-antihypertensive dose of eplerenone or (4) combined amlodipine and eplerenone for 6 weeks, and the effects on cardiovascular injuries were compared. There was no significant difference among the four groups regarding plasma aldosterone, urine volume or urinary electrolytes. A subpressor dose of eplerenone markedly ameliorated vascular endothelial dysfunction, cardiac inflammation and fibrosis in DS rats to a similar degree as an antihypertensive dose of amlodipine. Addition of eplerenone to amlodipine, without affecting blood pressure, enhanced the improvement by amlodipine of vascular endothelial function, cardiac inflammation, fibrosis and diastolic dysfunction in DS rats. Additive beneficial effects of eplerenone were attributed to additive potentiation of eNOS and Akt phosphorylation and additive reduction of oxidative stress. Eplerenone significantly attenuated cardiovascular NADPH oxidase activity by reducing gp91(phox) upregulation and attenuated the upregulation of cardiovascular AT1 receptor, but amlodipine failed to affect them. Thus, the normalization by eplerenone of gp91(phox) and AT1 receptor upregulation seems to be at least partially responsible for the additive benefits of eplerenone in the prevention of hypertensive cardiovascular injury. The combination of amlodipine and eplerenone may be a promising therapeutic strategy for cardiovascular disease in salt-sensitive hypertension.
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- 2011
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9. Benidipine, a dihydropyridine L-type/T-type calcium channel blocker, affords additive benefits for prevention of cardiorenal injury in hypertensive rats.
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Yamamoto E, Kataoka K, Dong YF, Nakamura T, Fukuda M, Nako H, Ogawa H, and Kim-Mitsuyama S
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- Animals, Blood Pressure, Calcium Channel Blockers pharmacology, Dihydropyridines pharmacology, Enzyme-Linked Immunosorbent Assay, Heart Rate, Male, Rats, Rats, Inbred SHR, Rats, Inbred WKY, Calcium Channel Blockers therapeutic use, Dihydropyridines therapeutic use, Heart drug effects, Hypertension complications, Kidney drug effects
- Abstract
Objectives: Benidipine is a dihydropyridine calcium channel blocker inhibiting not only L-type but also T-type calcium channels. To elucidate potential additive benefit of benidipine for prevention of cardiorenal injury, we compared the cardiac and renal protective effects of equihypotensive doses of benidipine and cilnidipine in stroke-prone spontaneously hypertensive rats (SHRSP)., Methods: SHRSP were divided into five groups, and were given vehicle, benidipine at 1 or 3 mg/kg per day, or cilnidipine at 1 or 3 mg/kg per day for 7 weeks, and the protective effects against cardiorenal injury were compared among each group., Results: Benidipine and cilnidipine at the same doses exerted comparable hypotensive effects on SHRSP throughout the treatment. Despite equihypotensive effects between both drugs, benidipine prevented cardiac hypertrophy, fibrosis, and inflammation to a greater extent than cilnidipine. Moreover, benidipine prevented glomerulosclerosis, tubulointerstitial injury, and renal inflammation more than cilnidipine. To elucidate the underlying mechanism of more beneficial effects of benidipine than cilnidipine, we compared the effects of these drugs on cardiac and renal oxidative stress, and aldosterone in SHRSP. Benidipine reduced both cardiac and renal NADPH oxidase activities in SHRSP more than cilnidipine, being associated with more attenuation of cardiac and renal superoxide by benidipine. Furthermore, serum aldosterone was significantly reduced by benidipine but not by cilnidipine., Conclusion: Benidipine exerted more protective effects against cardiorenal injury of hypertensive rats than cilnidipine, through more attenuation of oxidative stress than cilnidipine, and the reduction of aldosterone. Benidipine, via blockade of T-type calcium channels, seems to elicit additive benefits for prevention of hypertensive cardiorenal injury.
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- 2010
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10. Beneficial effects of pioglitazone on hypertensive cardiovascular injury are enhanced by combination with candesartan.
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Nakamura T, Yamamoto E, Kataoka K, Yamashita T, Tokutomi Y, Dong YF, Matsuba S, Ogawa H, and Kim-Mitsuyama S
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- Animals, Biphenyl Compounds, Blood Pressure drug effects, Blood Vessels enzymology, Cardiomegaly etiology, Cardiomegaly prevention & control, Cardiovascular Diseases etiology, Drug Combinations, Drug Synergism, Endothelium, Vascular physiopathology, Genetic Predisposition to Disease, Hypertension metabolism, Hypertension physiopathology, Male, Myocardium enzymology, Myocardium metabolism, NADPH Oxidase 1, NADPH Oxidases antagonists & inhibitors, Nitric Oxide Synthase Type III metabolism, Pioglitazone, Rats, Rats, Inbred SHR genetics, Rats, Inbred WKY, Reactive Oxygen Species antagonists & inhibitors, Stroke genetics, Superoxides metabolism, Ventricular Remodeling drug effects, rac1 GTP-Binding Protein antagonists & inhibitors, Angiotensin-Converting Enzyme Inhibitors pharmacology, Benzimidazoles pharmacology, Cardiovascular Diseases prevention & control, Hypertension complications, PPAR gamma agonists, Tetrazoles pharmacology, Thiazolidinediones pharmacology
- Abstract
The effect of pioglitazone, a peroxisome proliferator-activated receptor gamma agonist, on hypertensive cardiovascular injury is unknown. We examined the effect of pioglitazone on hypertensive cardiovascular injury and the significance of combination of pioglitazone with angiotensin type 1 receptor blocker. Stroke-prone spontaneously hypertensive rats (SHRSP) were orally given pioglitazone, candesartan, or combined pioglitazone and candesartan for 4 weeks to compare their effects on cardiovascular injury. Pioglitazone, without lowering blood pressure, significantly suppressed cardiac inflammation and fibrosis and reduced vascular endothelial dysfunction, and these beneficial effects were associated with the reduction of superoxide by inhibition of cardiovascular NADPH oxidase. Thus, pioglitazone protects against hypertensive cardiovascular injury, by inhibiting reactive oxygen species (ROS). Combination of pioglitazone and candesartan suppressed cardiac hypertrophy, inflammation, and interstitial fibrosis of SHRSP to a greater extent than either monotherapy, and reduced vascular endothelial dysfunction of SHRSP more than either monotherapy. Furthermore, more beneficial effects of their combination on cardiovascular injury were associated with more reduction of NADPH oxidase-mediated cardiovascular ROS. To elucidate the underlying molecular mechanism, we examined cardiovascular NADPH oxidase subunits. Pioglitazone monotherapy significantly attenuated cardiovascular p22(phox) and Rac1 in SHRSP, whereas pioglitazone combined with candesartan more attenuated p22(phox) and significantly reduced Nox1. Thus, additive suppression of cardiovascular NADPH oxidase by the combination was attributed to its additive attenuation of p22(phox) and Nox1 protein levels. In conclusion, we showed that pioglitazone protected against hypertensive cardiovascular damage, and the combination of pioglitazone and candesartan exerted more beneficial effects on hypertensive cardiovascular injury by more suppressing ROS.
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- 2008
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11. Novel mechanism and role of angiotensin II induced vascular endothelial injury in hypertensive diastolic heart failure.
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Yamamoto E, Kataoka K, Shintaku H, Yamashita T, Tokutomi Y, Dong YF, Matsuba S, Ichijo H, Ogawa H, and Kim-Mitsuyama S
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- Acetophenones pharmacology, Acetophenones therapeutic use, Amlodipine pharmacology, Amlodipine therapeutic use, Angiotensin II Type 1 Receptor Blockers pharmacology, Angiotensin II Type 1 Receptor Blockers therapeutic use, Animals, Antihypertensive Agents pharmacology, Antihypertensive Agents therapeutic use, Biopterins analogs & derivatives, Biopterins pharmacology, Biopterins therapeutic use, Blood Pressure, Calcium Channel Blockers pharmacology, Calcium Channel Blockers therapeutic use, Disease Models, Animal, Endothelium, Vascular drug effects, Endothelium, Vascular enzymology, Endothelium, Vascular pathology, Endothelium, Vascular physiopathology, Heart Failure, Diastolic drug therapy, Heart Failure, Diastolic etiology, Heart Failure, Diastolic pathology, Heart Failure, Diastolic physiopathology, Hydralazine pharmacology, Hydralazine therapeutic use, Hypertension drug therapy, Hypertension metabolism, Hypertension pathology, Hypertension physiopathology, MAP Kinase Kinase Kinase 5 antagonists & inhibitors, MAP Kinase Kinase Kinase 5 genetics, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, NADPH Oxidases metabolism, Rats, Rats, Inbred Dahl, Receptor, Angiotensin, Type 1 drug effects, Signal Transduction, Sodium Chloride, Dietary administration & dosage, Superoxides metabolism, Tetrazoles pharmacology, Tetrazoles therapeutic use, Time Factors, Valine analogs & derivatives, Valine pharmacology, Valine therapeutic use, Valsartan, Vasodilation, Angiotensin II metabolism, Apoptosis drug effects, Endothelium, Vascular metabolism, Heart Failure, Diastolic metabolism, Hypertension complications, MAP Kinase Kinase Kinase 5 metabolism, Nitric Oxide Synthase Type III metabolism, Receptor, Angiotensin, Type 1 metabolism
- Abstract
Objective: The mechanism and role of angiotensin II-induced vascular endothelial injury is unclear. We examined the molecular mechanism of angiotensin (AII)-induced vascular endothelial injury and its significance for hypertensive diastolic heart failure., Methods and Results: We compared the effect of valsartan and amlodipine on Dahl salt-sensitive hypertensive rats (DS rats). Valsartan improved vascular endothelial dysfunction of DS rats more than amlodipine, by inhibiting endothelial apoptosis and eNOS uncoupling more. Moreover, valsartan inhibited vascular apoptosis signal-regulating kinase 1 (ASK1) more than amlodipine. Thus, AT1 receptor contributed to vascular endothelial apoptosis, eNOS uncoupling, and ASK1 activation of DS rats. Using ASK1(-/-) mice, we examined the causative role of ASK1 in endothelial apoptosis and eNOS uncoupling. AII infusion in wild-type mice markedly caused vascular endothelial apoptosis and eNOS uncoupling accompanied by vascular endothelial dysfunction, whereas these effects of AII were absent in ASK1(-/-) mice. Therefore, ASK1 participated in AII-induced vascular endothelial apoptosis and eNOS uncoupling. Using tetrahydrobiopterin, we found that eNOS uncoupling was involved in vascular endothelial dysfunction in DS rats with established diastolic heart failure., Conclusions: AII-induced vascular endothelial apoptosis and eNOS uncoupling were mediated by ASK1 and contributed to vascular injury in diastolic heart failure of salt-sensitive hypertension.
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- 2007
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12. Pioglitazone exerts protective effects against stroke in stroke-prone spontaneously hypertensive rats, independently of blood pressure.
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Nakamura T, Yamamoto E, Kataoka K, Yamashita T, Tokutomi Y, Dong YF, Matsuba S, Ogawa H, and Kim-Mitsuyama S
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- Animals, Blood Glucose drug effects, Blood Glucose physiology, Blood Pressure drug effects, Blood Pressure physiology, Cerebral Arteries drug effects, Cerebral Arteries metabolism, Cerebral Arteries physiopathology, Cytokines drug effects, Cytokines metabolism, Diabetes Complications physiopathology, Disease Models, Animal, Endothelial Cells drug effects, Endothelial Cells metabolism, Hypertension physiopathology, Hypoglycemic Agents pharmacology, Hypoglycemic Agents therapeutic use, Macrophages drug effects, Macrophages metabolism, Male, Microcirculation drug effects, Microcirculation metabolism, Microcirculation physiopathology, NADH, NADPH Oxidoreductases antagonists & inhibitors, NADH, NADPH Oxidoreductases metabolism, NADPH Oxidase 1, Neuroprotective Agents therapeutic use, Oxidative Stress drug effects, Oxidative Stress physiology, Pioglitazone, Rats, Rats, Inbred SHR, Rats, Inbred WKY, Stroke etiology, Superoxides antagonists & inhibitors, Superoxides metabolism, Thiazolidinediones therapeutic use, Treatment Outcome, Hypertension complications, Neuroprotective Agents pharmacology, Stroke drug therapy, Stroke physiopathology, Thiazolidinediones pharmacology
- Abstract
Background and Purpose: Very recent subgroup analysis from the PROspective pioglitAzone Clinical Trial In macroVascular Events has shown that pioglitazone reduces the risk of recurrent stroke in type 2 diabetic patients. However, the underlying mechanism of stroke prevention by pioglitazone is unknown. Our aim was to examine the effect of pioglitazone on hypertension-based stroke in rats., Methods: Pioglitazone (1 mg x kg(-1) x d(-1)) was orally administered to stroke-prone spontaneously hypertensive rats (SHRSP) to examine the effect on incidental stroke, cerebrovascular injury, brain inflammation, oxidative stress, and vascular endothelial dysfunction induced by hypertension., Results: Treatment of SHRSP with pioglitazone for 4 weeks, without affecting blood pressure and blood glucose values, improved vascular endothelial dysfunction (P<0.05), suppressed remodeling of the middle cerebral artery (P<0.05) and brain microvessels (P<0.05), and inhibited brain macrophage infiltration (P<0.05) and the upregulation of brain monocyte chemoattractant protein-1 and tumor necrosis factor-alpha expression (P<0.01). Furthermore, pioglitazone treatment significantly delayed the onset of stroke signs and death in SHRSP (P<0.05). These beneficial effects of pioglitazone on cerebrovascular injury and stroke in SHRSP were associated with a reduction of brain and vascular superoxide via the inhibition of NADPH oxidase activity., Conclusions: Our work provides the first evidence that pioglitazone significantly protects against hypertension-induced cerebrovascular injury and stroke by improving vascular endothelial dysfunction, inhibiting brain inflammation, and reducing oxidative stress. These beneficial effects of pioglitazone were independent of blood pressure or blood sugar values. Thus, pioglitazone appears to be a potential therapeutic agent for stroke in type 2 diabetes with hypertension.
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- 2007
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13. Role of xanthine oxidoreductase in the reversal of diastolic heart failure by candesartan in the salt-sensitive hypertensive rat.
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Yamamoto E, Kataoka K, Yamashita T, Tokutomi Y, Dong YF, Matsuba S, Ogawa H, and Kim-Mitsuyama S
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- Acetophenones pharmacology, Animals, Biphenyl Compounds, Blood Pressure drug effects, Blood Pressure physiology, Cardiac Output, Low etiology, Cardiac Output, Low physiopathology, Heart Ventricles drug effects, Heart Ventricles metabolism, Hypertension complications, Hypertension physiopathology, Liver drug effects, Lung drug effects, Mitogen-Activated Protein Kinase Kinases metabolism, Myocardium metabolism, NADPH Oxidases antagonists & inhibitors, NADPH Oxidases metabolism, Oxypurinol pharmacology, Rats, Rats, Inbred Dahl, Reactive Oxygen Species metabolism, Xanthine Oxidase antagonists & inhibitors, Angiotensin II Type 1 Receptor Blockers therapeutic use, Benzimidazoles therapeutic use, Cardiac Output, Low drug therapy, Hypertension drug therapy, Tetrazoles therapeutic use, Xanthine Oxidase metabolism
- Abstract
The role of angiotensin II and reactive oxygen species in the exacerbation of diastolic heart failure is unknown. We examined the therapeutic effect of angiotensin blockade on hypertensive diastolic heart failure, focusing on the role of xanthine oxidoreductase and reduced nicotinamide-adenine dinucleotide phosphate oxidase, major enzymes producing reactive oxygen species. Dahl salt-sensitive hypertensive rats (DS rats) with established diastolic heart failure were given vehicle, candesartan (an angiotensin II receptor subtype 1 receptor blocker), oxypurinol (a xanthine oxidoreductase inhibitor), apocynin (a reduced nicotinamide-adenine dinucleotide phosphate oxidase inhibitor), or hydralazine (a vasodilator), and their therapeutic effects on diastolic heart failure were compared. Candesartan treatment of DS rats with established diastolic heart failure reversed cardiac remodeling, improved cardiac relaxation abnormality, and prolonged survival, being accompanied by the attenuation of the increase in cardiac superoxide, reduced nicotinamide-adenine dinucleotide phosphate oxidase, and xanthine oxidoreductase activities. Thus, the beneficial effect of candesartan in DS rats appears to be mediated by the inhibition of cardiac reactive oxygen species. Cardiac xanthine oxidoreductase inhibition with oxypurinol significantly reduced cardiac superoxide, prevented the progression of cardiac remodeling, and delayed the mortality in DS rats. Apocynin, which significantly inhibited cardiac reduced nicotinamide-adenine dinucleotide phosphate oxidase activity, prevented the exacerbation of diastolic heart failure more than hydralazine. However, compared with candesartan or oxypurinol, apocynin did not improve cardiac reactive oxygen species, remodeling, and function in DS rats. In conclusion, candesartan slowed the exacerbation of hypertensive diastolic heart failure in DS rats by causing reverse cardiac remodeling. Cardiac xanthine oxidoreductase contributed to these beneficial effects of candesartan.
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- 2007
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14. Pravastatin enhances beneficial effects of olmesartan on vascular injury of salt-sensitive hypertensive rats, via pleiotropic effects.
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Yamamoto E, Yamashita T, Tanaka T, Kataoka K, Tokutomi Y, Lai ZF, Dong YF, Matsuba S, Ogawa H, and Kim-Mitsuyama S
- Subjects
- Animals, Disease Models, Animal, Drug Interactions, Drug Therapy, Combination, Endothelium, Vascular pathology, Hypertension drug therapy, Nitric Oxide blood, Nitric Oxide metabolism, Oxidative Stress drug effects, Rats, Rats, Inbred Dahl, Reference Values, Risk Factors, Sensitivity and Specificity, Sodium Chloride, Dietary administration & dosage, Vascular Diseases etiology, Endothelium, Vascular drug effects, Hydroxymethylglutaryl-CoA Reductase Inhibitors pharmacology, Hypertension complications, Imidazoles pharmacology, Oxidation-Reduction drug effects, Pravastatin pharmacology, Tetrazoles pharmacology, Vascular Diseases prevention & control
- Abstract
Objective: This work was undertaken to investigate comparative effect of AT1 receptor blocker (ARB), 3-hydroxy-3-methylglutaryl (HMG) coenzymeA (CoA) reductase inhibitor (statin), and their combination on vascular injury of salt-sensitive hypertension., Methods and Results: Salt-loaded Dahl salt-sensitive hypertensive rats (DS rats) were treated with (1) vehicle, (2) hydralazine (5 mg/kg/d), (3) olmesartan (0.5 mg/kg/d), (4) pravastatin (100 mg/kg/d), and (5) combined olmesartan and pravastatin for 4 weeks. Olmesartan or pravastatin significantly and comparably improved vascular endothelium-dependent relaxation to acetylcholine, coronary arterial remodeling, and eNOS activity of DS rats. Olmesartan prevented vascular eNOS dimer disruption or the downregulation of dihydrofolate reductase (DHFR) more than pravastatin, whereas Akt phosphorylation was enhanced by pravastatin but not olmesartan, indicating differential pleiotropic effects between olmesartan and pravastatin. Add-on pravastatin significantly enhanced the improvement of vascular endothelial dysfunction and remodeling by olmesartan in DS rats. Moreover, pravastatin enhanced the increase in eNOS activity by olmesartan, being associated with additive effects of pravastatin on phosphorylation of Akt and eNOS., Conclusions: Olmesartan and pravastatin exerted beneficial vascular effects in salt-sensitive hypertension, via differential pleiotropic effects. Pravastatin enhanced vascular protective effects of olmesartan. Thus, the combination of ARB with statin may be the potential therapeutic strategy for vascular diseases of salt-sensitive hypertension.
- Published
- 2007
- Full Text
- View/download PDF
15. The impact of superselective adrenal artery embolization on renal function in patients with primary aldosteronism: a prospective cohort study
- Author
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Lai, Ze-Qun, Fu, Yang, Liu, Jian-Wei, Zhang, Hong-Jin, Zhang, Huang, Liang, Ning-Peng, and Dong, Yi-Fei
- Published
- 2024
- Full Text
- View/download PDF
16. Superselective adrenal arterial embolization for primary aldosteronism without lateralized aldosterone secretion: an efficacy and safety, proof-of-principle study
- Author
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Qiu, Jian, Li, Ning, Xiong, Hong-Liang, Yang, Jiao, Li, Yun-De, Hu, Chen-Kai, Lai, Ze-Qun, Liang, Ning-Peng, Zhang, Hong-Jin, Jiang, Xiong-Jing, and Dong, Yi-Fei
- Published
- 2023
- Full Text
- View/download PDF
17. Advances in research on blood pressure regulation by clock gene PER
- Author
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JI Hui-fang, FU Yang, DONG Yi-fei
- Subjects
per ,blood pressure circadian rhythm ,hypertension ,chronotherapy ,Medicine - Abstract
The abnormal expression of clock genes is closely related to the circadian rhythm of blood pressure and to the occurrence and development of hypertension. This article summarizes the relationship between the clock gene period (PER) and the circadian rhythm of blood pressure, the influence of abnormal expression of PER in peripheral tissues and organs related to blood pressure regulation on blood pressure, and the research progress in the field of hypertension chronotherapy. The author hopes to provide new ideas for the clinical diagnosis, treatment and prognosis of hypertension.
- Published
- 2022
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- View/download PDF
18. Significant interaction of hypertension and homocysteine on neurological severity in first-ever ischemic stroke patients.
- Author
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Fan, Ying-Li, Zhan, Rui, Dong, Yi-Fei, Huang, Lei, Ji, Xi-Xin, Lu, Peng, Liu, Jian, Li, Ping, and Cheng, Xiao-Shu
- Abstract
It is not known whether combination of hypertension and high homocysteine (HHcy) impacts on stroke-related neurological severity. Our aim was to determine whether there is an interaction of hypertension and HHcy on neurological severity in first-ever ischemic stroke patients. We analyzed neurological severity among 189 consecutive first-ever ischemic stroke patients with or without hypertension or HHcy. Hypertension (odds ratio [OR]: 8.086, 95% confidence interval [CI]: 3.596–18.181, P < .001) and total homocysteine (OR: 1.403, 95% CI: 1.247–1.579, P < .001) were independently associated with neurological severity. In receiver-operating characteristic analysis, total homocysteine was a significant predictor of neurological severity (area under curve: 0.794; P < .001). A multiplicative interaction of hypertension and HHcy on more severe neurological severity was revealed by binary logistic regression (OR: 13.154, 95% CI: 5.293–32.691, P < .001). Analysis further identified a more than multiplicative interaction of hypertension and HHcy on neurological severity compared with patients without each condition (OR: 50.600, 95% CI: 14.775–173.285, P < .001). Interaction effect measured on an additive scale showed that 76.4% patients with moderate/severe neurological severity were attributed to interaction of hypertension and HHcy. Significant interaction of hypertension and HHcy on neurological severity was found on multiplicative and additive scale in first-ever Chinese ischemic stroke patients. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
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