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Hypertension. 1995 Mar;25(3):437-42.
Cardiovascular changes by long-term inhibition of the renin-angiotensin system in aging.

Inserra F, Romano L, Ercole L, de Cavanagh EM, Ferder L.

Institute of Nephrology, Jewish Hospital, Buenos Aires, Argentina.

We studied four groups of 20 female mice to evaluate the long-term effect of an angiotensin-converting enzyme on myocardium and vessels during the natural process of aging. Three groups received enalapril in water from weaning to 24 months of age (group A, 20 mg/L; group B, 10 mg/L; group C, 5 mg/L); group D served as a control. Animals surviving after 24 months were killed, and morphometric studies were performed. Total corporal weight was higher in animals receiving enalapril. Cardiac weight relative to total body weight was lower in the treated groups than in the control group. Cardiac morphometric studies showed lower myocardiosclerosis in animals receiving angiotensin-converting enzyme inhibitor (groups A through D, respectively, 0.9 +/- 0.6%, 1.1 +/- 0.2%, 1.03 +/- 0.1%, and 9.5 +/- 4.3%; P < .01, groups A, B, and C versus D). The number of mitochondria per myocardiocyte was higher in the groups receiving enalapril (A through D, respectively, 85 +/- 7, 85 +/- 6, 83 +/- 8, and 58 +/- 8; P < .01, groups A, B, and C versus D). At the vascular level, vessel diameters were not significantly different between the groups receiving angiotensin-converting enzyme inhibitor and the control group, whereas differences were seen in arterial tunica media thickness (wall-lumen ratio) (groups A through D, respectively, aorta: 0.13 +/- 0.02, 0.11 +/- 0.02, 0.12 +/- 0.01, 2.81 +/- 0.35; intrapulmonary: 0.9 +/- 0.43, 0.6 +/- 0.41, 0.8 +/- 0.46, 1.9 +/- 0.51; intracerebral: 2.18 +/- 0.46, 2.29 +/- 0.45, 2.46 +/- 0.43, 3.30 +/- 0.41; intrarenal: 2.28 +/- 0.46, 2.73 +/- 0.48, 2.70 +/- 0.51, 3.23 +/- 0.41; intracariaciac: 2.27 +/- 0.44, 2.59 +/- 0.41, 2.80 +/- 0.43, 3.68 +/- 0.47; P < .001, groups A, B, and C versus D).(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7875769&dopt=Abstract




Drugs. 1988;35 Suppl 5:62-71.
Renal protective effect of long term antihypertensive therapy with enalapril.

Bauer JH, Reams GP.

Department of Medicine, University of Missouri School of Medicine, Columbia.

This review focuses on recent human studies with the angiotensin-converting enzyme (ACE) inhibitor enalapril, prescribed either alone or in combination with a diuretic, to patients with essential hypertension and to patients with hypertension associated with moderate to severe renal parenchymal disease. Data suggest that enalapril therapy may provide a renal protective effect. In addition to lowering and controlling systemic arterial blood pressure, enalapril therapy is associated with stabilisation of, and/or improvement in effective renal plasma flow, glomerular filtration rate (GFR) and urinary protein excretion. Such renal protective effects are probably mediated by normalisation of both the systemic arterial blood pressure and intraglomerular capillary hydraulic pressure, and by an increase in the glomerular ultrafiltration coefficient. Drug therapy enabling control of both systemic and glomerular hypertension may prevent hypertensive renal end-organ damage and attenuate the natural progression of renal parenchymal disease.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2850905&dopt=Abstract




Hypertension. 1997 Jun;29(6):1260-4.
Effects of enalapril, losartan, and verapamil on blood pressure and glucose metabolism in the Cohen-Rosenthal diabetic hypertensive rat.

Rosenthal T, Erlich Y, Rosenmann E, Cohen A.

Chorley Institute of Hypertension, Chaim Sheba Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Hashomer, Israel.

We undertook the present study to examine the effect of the angiotensin-converting enzyme inhibitor enalapril, the angiotensin II antagonist losartan, and calcium antagonist verapamil on systolic pressure and spontaneous blood glucose levels in rats from the Cohen-Rosenthal diabetic hypertensive strain. Genetic hypertension and diabetes developed in this strain after crossbreeding of Cohen diabetic and spontaneously hypertensive rats. The new rat strain was fed their usual copper-poor sucrose diet, which is essential for the development of this model, and for 4 weeks received either enalapril, losartan, or verapamil. Systolic pressure was reduced significantly compared with controls in all treated groups. Chronic treatment with enalapril or verapamil, but not with losartan, succeeded in lowering spontaneous blood glucose, indicating improved diabetic control. Data suggest that angiotensin-converting enzyme inhibition by enalapril, but not angiotensin II antagonism by losartan, can improve glucose metabolism in addition to its hypotensive effect in a genetic diabetic hypertensive rat strain. This confirms that the drop in glucose with converting enzyme inhibition is highly dependent on bradykinin accumulation. Data further suggest that calcium channel blockade by verapamil can also improve glucose metabolism. The question remains whether the reduction in glucose by verapamil was a result of inhibition of glucogenesis.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9180626&dopt=Abstract












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