10 results on '"Mann JF"'
Search Results
2. Safety of the combination of valsartan and benazepril in patients with chronic renal disease. European Group for the Investigation of Valsartan in Chronic Renal Disease.
- Author
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Ruilope LM, Aldigier JC, Ponticelli C, Oddou-Stock P, Botteri F, and Mann JF
- Published
- 2000
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3. Effects of angiotensin converting enzyme inhibitor on renal haemodynamics during mental stress.
- Author
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Schmieder RE, Schobel HP, Gatzka CE, Häuser W, Dominiak P, Mann JF, Luft FC, Schmieder, R E, Schobel, H P, Gatzka, C E, Häuser, W, Dominiak, P, Mann, J F, and Luft, F C
- Published
- 1996
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4. LEADER-4: blood pressure control in patients with type 2 diabetes and high cardiovascular risk: baseline data from the LEADER randomized trial.
- Author
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Petrie JR, Marso SP, Bain SC, Franek E, Jacob S, Masmiquel L, Leiter LA, Haluzik M, Satman I, Omar M, Shestakova M, Van Gaal L, Mann JF, Baeres FM, Zinman B, and Poulter NR
- Subjects
- Aged, Antihypertensive Agents therapeutic use, Blood Pressure, Diabetes Mellitus, Type 2 complications, Double-Blind Method, Female, Glucagon-Like Peptide-1 Receptor antagonists & inhibitors, Humans, Hypertension complications, Liraglutide adverse effects, Male, Middle Aged, North America, Risk Factors, Diabetes Mellitus, Type 2 drug therapy, Diabetes Mellitus, Type 2 physiopathology, Hypertension drug therapy, Hypertension physiopathology, Hypoglycemic Agents therapeutic use, Liraglutide therapeutic use
- Abstract
Objective: As glucagon-like peptide-1 receptor agonists lower blood pressure (BP) in type 2 diabetes mellitus (T2DM), we examined BP control in relation to targets set by international bodies prior to randomization in the Liraglutide Effect and Action in Diabetes: Evaluation of cardiovascular outcome Results (LEADER) trial., Methods: We analyzed baseline data from LEADER (NCT01179048), an ongoing phase 3B, randomized, double-blind, placebo-controlled cardiovascular outcomes trial examining the cardiovascular safety of the glucagon-like peptide-1 receptor agonist liraglutide in 9340 people with T2DM from 32 countries [age (all mean ± SD) 64 ± 7.2 years, BMI 32.5 ± 6.3 kg/m, duration of diabetes 12.7 ± 8.0 years], all of whom were at high risk for cardiovascular disease (CVD)., Results: A total of 81% (n = 7592) of participants had prior CVD and 90% (n = 8408) had a prior history of hypertension. Despite prescription of multiple antihypertensive agents at baseline, only 51% were treated to a target BP of less than 140/85 mmHg and only 26% to the recommended baseline BP target of less than 130/80 mmHg. In univariate analyses, those with prior CVD were prescribed more agents (P < 0.001) and had lower BP than those without (137 ± 18.8/78 ± 10.6 mmHg versus 140 ± 17.7/80 ± 9.9 mmHg; P < 0.001). In logistic regression analyses, residency in North America (64% treated to <140/85 mmHg; 38% treated to <130/80 mmHg) was the strongest predictor of BP control., Conclusion: These contemporary data confirm that BP remains insufficiently controlled in a large proportion of individuals with T2DM at high cardiovascular risk, particularly outside North America. Longitudinal data from the LEADER trial may provide further insights into BP control in relation to cardiovascular outcomes in this condition.
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- 2016
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5. Vascular conversion of angiotensin I in stroke-prone spontaneously hypertensive and Wistar-Kyoto rats.
- Author
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Hilgers KF, Veelken R, Mai M, Ganten U, Ganten D, Luft FC, and Mann JF
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- Aging blood, Aging physiology, Animals, Cerebrovascular Disorders, Chromatography, High Pressure Liquid, Hindlimb blood supply, Hypertension genetics, Hypertension physiopathology, Male, Radioimmunoassay, Rats, Rats, Inbred SHR physiology, Rats, Inbred WKY physiology, Angiotensin I blood, Angiotensin II blood, Hypertension blood, Rats, Inbred SHR blood, Rats, Inbred SHR genetics, Rats, Inbred WKY blood
- Abstract
Objective: Linkage studies have shown that the gene locus for angiotensin converting enzyme (ACE) is associated with the expression of hypertension in stroke-prone spontaneously hypertensive rats (SHRSP). We tested the hypothesis that the conversion of angiotensin I (Ang I) to angiotensin II (Ang II) in blood vessels is elevated in SHRSP., Design: We measured the conversion rate of Ang I to Ang II during one pass through an isolated resistance vessel bed. We used the same substrains of SHRSP and Wistar-Kyoto control rats (WKY) that had been employed in the earlier linkage studies., Methods: Isolated hindquarters from young and adult (10- to 12- and 36- to 38-week-old) rats were perfused with an artificial medium and then infused with Ang I at 0.5 and 2 pmol/ml. Ang I and II were measured with high-performance liquid chromatography and radioimmunoassay in hindquarter effluent and in blank control channels. Conversion and extraction rates were calculated from angiotensin levels in hindquarter and blank perfusion channels, respectively., Results: The conversion rates of Ang I to Ang II did not differ between SHRSP and WKY in young or in adult rats. Captopril completely abolished the formation of Ang II in all groups of rats. During infusion at the higher dose of Ang I, the extraction of Ang I was significantly decreased in SHRSP compared with WKY., Conclusions: Our results are consistent with the notion that the metabolism of angiotensin is decreased in spontaneously hypertensive rats. However, we found no support for the hypothesis that vascular ACE is responsible for high blood pressure in SHRSP. These findings suggest that other genes close to the ACE locus or the hyperexpression of the enzyme in other areas may contribute to hypertension in these rats.
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- 1993
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6. Local angiotensin formation in hindlimbs of uremic hypertensive and renovascular hypertensive rats.
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Kuczera M, Hilgers KF, Lisson C, Ganten D, Hilgenfeldt U, Ritz E, and Mann JF
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- Angiotensin II metabolism, Angiotensinogen metabolism, Animals, Chromatography, High Pressure Liquid, Hindlimb, Male, Radioimmunoassay, Rats, Rats, Inbred Strains, Angiotensin II biosynthesis, Blood Vessels metabolism, Hypertension, Renal metabolism, Hypertension, Renovascular metabolism, Renin physiology, Renin-Angiotensin System physiology, Uremia metabolism
- Abstract
To examine and characterize the vascular renin--angiotensin system in low-renin models of renal hypertension with and without the presence of overt renal insufficiency, we studied the formation and metabolism of angiotensin in isolated perfused rat hindquarter preparations. Rats with 5/6 nephrectomy (5/6NX) and rats with one-kidney, one clip (1K1C) hypertension were compared to sham operated (sham) animals. Angiotensin peptides in plasma or perfusate were characterized by high-performance liquid chromatography and radioimmunoassay (RIA). Plasma angiotensin II was lower, and blood pressure was higher in both experimental groups, compared to sham animals. Plasma angiotensinogen, measured by both direct and indirect RIA, was increased in both experimental groups. The spontaneous release of angiotensin I and angiotensin II from perfused hindquarters did not differ between the groups. Angiotensin I conversion was not different in 5/6NX or 1K1C groups compared with controls. Furthermore, angiotensin conversion was completely inhibited by captopril (1 mumol/l) in all groups. Renin-induced angiotensin release was significantly increased in 5/6NX as compared with sham rats, whereas there was no difference in renin-induced angiotensin release between 1K1C and sham animals. Angiotensin II degradation was significantly attenuated in 5/6NX rats when compared with sham rats (27.6% versus 53.9%, respectively, P less than 0.05) but was unaltered in 1K1C rats. Thus, in chronic uremic hypertension, renin-induced angiotensin formation was increased in the face of decreased angiotensin II degradation. These data suggest that vascular angiotensin may contribute to the elevated blood pressure observed in chronic renal failure. In 1K1C rats, vascular angiotensin formation and metabolism was unchanged despite suppressed plasma angiotensin II.
- Published
- 1991
7. Natriuresis-pressure relationship in polycystic kidney disease.
- Author
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Schmid M, Mann JF, Stein G, Herter M, Nussberger J, Klingbeil A, and Ritz E
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- Adult, Angiotensin II blood, Atrial Natriuretic Factor blood, Body Weight drug effects, Female, Glomerular Filtration Rate drug effects, Humans, Hypertension etiology, Hypertension physiopathology, Male, Middle Aged, Polycystic Kidney Diseases blood, Polycystic Kidney Diseases complications, Receptors, Angiotensin blood, Sodium, Dietary administration & dosage, Sodium, Dietary pharmacology, Blood Pressure drug effects, Natriuresis drug effects, Polycystic Kidney Diseases physiopathology
- Abstract
We studied, under outpatient conditions, nine patients with autosomal dominant polycystic kidney disease who were hypertensive on their usual diet, and nine normotensive healthy probands. The subjects were examined in random order on the 7th day after equilibration on a low-sodium diet (20 mmol/day) and again on the 7th day after equilibration on the same diet but with added sodium to yield a final intake of 200 mmol/day (or vice versa). Blood pressure was monitored non-invasively for 2 h at 4-min intervals using an automatic system. In healthy probands, mean arterial pressure (MAP) was similar on the low- and the high-sodium diets (92.7 versus 91.9 mmHg). In hypertensive patients, a significant (P less than 0.02) increase in mean MAP (107.2 versus 111.2 mmHg) and in systolic blood pressure (140.6 versus 148.7 mmHg) was observed irrespective of whether the glomerular filtration rate (GFR) was normal or reduced. The natriuresis pressure curve showed an upward shift (resetting) and a positive slope (sodium sensitivity). Patients with a reduced GFR as shown by inulin clearance differed from probands and patients with a normal GFR, by showing greater proportional changes in GFR and body weight. In hypertensive patients, atrial natriuretic factor (ANF) levels were higher at baseline and showed an exaggerated response to sodium loading. Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. These data show a resetting of the natriuresis-blood pressure relationship and an increased blood pressure sensitivity to sodium in hypertensive patients with adult, dominant, polycystic kidney disease.
- Published
- 1990
8. Haemodynamic effects of intact digoxin antibody and its Fab fragments in experimental hypertension.
- Author
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Mann JF, Miemietz R, Ganten U, and Ritz E
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- Animals, Blood Pressure, Cardiac Output, Desoxycorticosterone, Digoxin administration & dosage, Female, Hypertension chemically induced, Male, Rats, Rats, Inbred SHR, Rats, Inbred Strains, Sodium, Dietary administration & dosage, Vascular Resistance, Digoxin immunology, Hemodynamics, Hypertension drug therapy, Immunoglobulin Fab Fragments immunology
- Abstract
The effects of i.v. injection of intact digoxin antibody (0.3 mg/rat) and of its Fab fragment (40 mg/rat) on blood pressure, cardiac output and total peripheral resistance were measured in conscious spontaneously hypertensive and deoxycorticosterone hypertensive rats. In vitro findings showed that Fab fragment bound radio-labelled digoxin, digitoxin and ouabain more efficiently than did intact antibody. In vivo, Fab fragment prevented the increase of total peripheral resistance induced by i.v. injection digoxin. However, Fab fragment of digoxin antibody did not alter blood pressure, cardiac output or total peripheral resistance in normal and salt-loaded spontaneously hypertensive rats (SHR) in uraemic SHR and in deoxycorticosterone hypertensive rats. We confirmed that intact digoxin antibody--bearing Fc domains with complement activating properties--lowered blood pressure in SHR and in deoxycorticosterone hypertension. This was due to a decrease in total peripheral resistance. Our data suggest that a circulating endogenous digitalis-like factor is unlikely to be important in blood pressure regulation in salt-loaded hypertension in the rat.
- Published
- 1987
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9. Angiotensin formation in the isolated rat hindlimb.
- Author
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Hilgers KF, Kuczera M, Wilhelm MJ, Wiecek A, Ritz E, Ganten D, and Mann JF
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- Angiotensin I isolation & purification, Angiotensin I metabolism, Angiotensin II isolation & purification, Angiotensin II metabolism, Angiotensin-Converting Enzyme Inhibitors, Animals, Captopril pharmacology, Chromatography, High Pressure Liquid, In Vitro Techniques, Male, Radioimmunoassay, Rats, Rats, Inbred Strains, Renin pharmacology, Vasoconstriction drug effects, Angiotensin I biosynthesis, Angiotensin II biosynthesis, Hindlimb metabolism
- Abstract
Local vascular generation of angiotensin was investigated in isolated perfused rat hindquarters. Extraction and combined high-performance liquid chromatography (HPLC)/radioimmunoassay analysis of hindlimb perfusate showed a spontaneous release of angiotensin I (Ang I; 5.0 +/- 3.4 fmol/h) and angiotensin II (Ang II; 31.8 +/- 7.9 fmol/h). Angiotensin converting enzyme (ACE) inhibition with captopril abolished Ang II release while Ang I levels increased more than 10-fold. Perfusion with purified hog renin caused a dose-dependent angiotensin release and vasoconstriction. The renin inhibitor H-142 abolished all effects of renin whereas ACE inhibition prevented Ang II formation and vasoconstriction but increased Ang I levels. Metabolism and pressor effects of synthetic tetradecapeptide renin substrate (TDP), Ang I and Ang II were studied using a recirculating rat hindlimb perfusion system. TDP-dependent formation of Ang I and II, and an increase in perfusion pressure was shown; ACE inhibition reduced but did not abolish Ang II formation and vasoconstriction. Ang I was converted to Ang II by about 50% during one pass through a hindlimb. This conversion was abolished by ACE inhibition. These data add support to the presence of a functional vascular renin-angiotensin system.
- Published
- 1989
- Full Text
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10. 125I-Angiotensin II binding to human blood cells.
- Author
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Mann JF, Sis J, and Ritz E
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- Humans, Kinetics, Angiotensin II metabolism, Blood Platelets metabolism, Receptors, Angiotensin metabolism, Receptors, Cell Surface metabolism
- Abstract
The binding of 125I-angiotensin II to human blood cells was investigated. Blood was drawn from healthy volunteers and platelets prepared with minimal contamination of red cells and white blood cells (less than 0.1%). Using thin layer chromatography, degradation of 125I-angiotensin II by platelets could be demonstrated in the presence of various enzyme inhibitors. However, when incubated with 1 mM diisopropylfluorophosphate (DFP) or 1 mg/ml bacitracin, no breakdown of 125I-angiotensin II could be detected. The amount of specifically bound 125I-angiotensin II increased linearly with the number of cells per tube. Binding reached a plateau within 90-120 min at 37 degrees C, and was stable thereafter. Specific binding was reversible. No binding could be detected at 4 degrees C. Specific binding of 125I-angiotensin II was saturable. Scatchard analysis of binding by platelets of healthy volunteers revealed one class of binding sites with an apparent Kd of 127 +/- 16 pM and a maximal binding capacity of 7.9 +/- 1.5 binding sites per cell. Competitive displacement of 125I-angiotensin II binding by angiotensin II-analogues showed a rank order of effectiveness. Unrelated peptides, e.g. bradykinin, vasopressin and enkephalin, did not displace specifically bound angiotensin II. Human mononuclear leucocytes were prepared by a Ficoll-isopaque gradient. However, these cells could not be used for studies of specific binding, since enzymatic degradation of 125I-angiotensin II could not be prevented despite addition of various enzyme inhibitors. Time-dependent uptake of 125I-angiotensin II showed no stable plateau. Thus our study shows specific binding of 125I-angiotensin II to human platelets.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1985
- Full Text
- View/download PDF
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