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      Differing Roles of Body Mass and the Renin-Angiotensin System in Mediating the Hypertension Syndrome


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          Background: Hypertension is characterized not only by a metabolic syndrome that includes obesity and insulin resistance, but also by increases in left-ventricular mass (LVM), reduced arterial compliance and altered renal function. This investigation has examined a possible role for the renin-angiotensin system as well as body mass and insulin values in mediating these cardiovascular and renal aspects of the hypertension syndrome. Methods: This was a cross-sectional study of 142 patients identified by community screening. Mean (±SE) age was 46 ± 1 years and patients had stage I–II hypertension (blood pressure: 145 ± 1/98 ± 0.5 mm Hg). For analysis, patients were divided into 2 groups: those with body mass index (BMI) <27 kg/m<sup>2</sup> (lean, n = 72) or BMI >27 kg/m<sup>2</sup> (overweight, n = 70). Results: By univariate analysis, LVM in lean patients correlated significantly with plasma renin activity (PRA), plasma aldosterone, BMI and systolic BP; but with multivariate regression, only PRA (p < 0.01) and BMI (p < 0.04) remained in the model as independent predictors of LVM. For LVM in overweight patients, only BMI (p < 0.02) remained in the model. For total arterial compliance (stroke volume/pulse pressure) only fasting plasma insulin (in the overweight group) was significantly related (p < 0.01). For urinary protein excretion, the only predictor in lean patients was PRA (p < 0.02), whereas in overweight patients it was BMI (p < 0.03). For creatinine clearance, BMI (p < 0.01 in overweight patients) remained in the model, though by univariate regression PRA had an age-dependent dichotomous relationship to clearance: r = +0.25 (p < 0.01) in patients <55 years, but r = –0.54 (p < 0.01) in patients ≥55 years. Conclusion: These findings suggest that in overweight patients cardiovascular and renal values depend chiefly on body weight and insulin, but that in normal weight hypertensives the renin-angiotensin system may play the major role.

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          Targeting TGF-beta overexpression in renal disease: maximizing the antifibrotic action of angiotensin II blockade.

          Overproduction of transforming growth factor-beta (TGF-beta) is a key mediator of extracellular matrix accumulation in fibrotic diseases. We hypothesized that the degree of reduction of pathological TGF-beta expression can be used as a novel index of the antifibrotic potential of angiotensin II (Ang II) blockade in renal disease. One day after induction of Thy 1.1 glomerulonephritis, rats were treated with increasing doses of the Ang I converting enzyme (ACE) inhibitor enalapril and/or the Ang II receptor blocker losartan in the drinking water. Six days after disease induction the therapeutic effect on glomerular TGF-beta overexpression was evaluated. Both enalapril and losartan reduced TGF-beta overproduction in a dose-dependent manner, showing a moderate reduction at doses known to control blood pressure in renal forms of hypertension. A maximal reduction in TGF-beta expression of approximately 45% was seen for both drugs starting at 100 mg/liter enalapril and 500 mg/liter losartan, with no further reduction at doses of enalapril up to 1000 mg/liter or losartan up to 2500 mg/liter. Co-treatment with both drugs was not superior to single therapy. Consistent with our hypothesis that reduction in TGF-beta expression is a valid target, other disease measures, including glomerular matrix accumulation, glomerular production and mRNA expression of the matrix protein fibronectin and the protease inhibitor plasminogen-activator-inhibitor type 1 (PAI-1) closely followed TGF-beta expression. The data suggest that these therapies act through very similar pathways and that, in order to more effectively treat renal fibrosis, these drugs must be combined with other drugs that act by different mechanisms.
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            Effects of angiotensin receptor antagonist and angiotensin converting enzyme inhibitor on insulin sensitivity in fructose-fed hypertensive rats and essential hypertensives.

            This study was designed to investigate the effects of angiotensin II (AII) receptor antagonist and angiotensin converting enzyme (ACE) inhibitor on insulin resistance, and the mechanism by which ACE inhibitor improves insulin-dependent glucose uptake (insulin sensitivity) in an insulin-resistant hypertensive rat model (fructose-fed rats, FFR) and in essential hypertensives (EHT). Male Sprague-Dawley rats were fed on fructose-rich or standard chow for 4 weeks and treated either with 10 mg/kg/day of delapril (n = 8), 1 mg/kg/day of TCV-116 (AII receptor antagonist; n = 13), or vehicle (n = 9) for the latter 2 weeks. Steady-state plasma glucose (SSPG) was measured with the subjects in the conscious state; simultaneously, we infused insulin (2.5 mU/kg/min) and glucose (8 mg/kg/min) to determine insulin sensitivity in each group. Thirteen EHT were hospitalized and the 2-h euglycemic hyperinsulinemic glucose clamp (GC) method was performed in a fasting condition before and after 2 weeks' administration of TCV-116 (8 mg/day) in 7 EHT and of delapril (120 mg/day) in 6 EHT. Insulin sensitivity was evaluated as M-value calculated from the infusion rate of glucose. Mean blood pressure (MBP) was higher in FFR (137.7 +/- 73.8 mm Hg, P < .05) compared to controls (120.8 +/- 2.7 mm Hg), and was lower in both the delapril (108.1 +/- 6.3 mm Hg, P < .05) and TCV-116 (112.8 +/- 4.3 mm Hg, P < .05) groups than in FFR.(ABSTRACT TRUNCATED AT 250 WORDS)

              Author and article information

              Am J Nephrol
              American Journal of Nephrology
              S. Karger AG
              June 2000
              30 June 2000
              : 20
              : 3
              : 169-174
              aThe Brookdale University Hospital, SUNY Health Science Center, Brooklyn, N.Y., bVA Medical Center, Long Beach, Calif., USA
              13579 Am J Nephrol 2000;20:169–174
              © 2000 S. Karger AG, Basel

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              Page count
              Figures: 2, Tables: 3, References: 23, Pages: 6
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/13579
              Self URI (text/html): https://www.karger.com/Article/FullText/13579
              Self URI (journal page): https://www.karger.com/SubjectArea/Nephrology
              Clinical Study

              Cardiovascular Medicine,Nephrology
              Renin,Hypertension,Left-ventricular mass,Renal function,Body mass index


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