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Am J Kidney Dis. 1996 Oct;28(4):603-9.
The urinary bladder angiotensin system: response to infusions of angiotensin I and angiotensin-converting enzyme inhibitors.

Weaver-Osterholtz D, Reams G, Wu Z, Knaus J, Campbell F, Bauer JH.

Department of Surgery, University of Missouri, Columbia, MO 65212, USA.

The circulating and urinary bladder tissue concentrations of angiotensin I (ANG I) and angiotensin II [ANG-(1-8)] were examined in anesthetized Sprague-Dawley male rats given an intravenous bolus infusion of either ANG I, the angiotensin-converting enzyme (ACE) inhibitors enalaprilat or ramiprilat, or saline. The mean concentrations of ANG I and ANG-(1-8) were markedly higher in the urinary bladder tissue than in whole blood. There was a significant increase in the concentration of ANG I and ANG-(1-8), both in the urinary bladder tissue and the circulation, after the ANG I infusion. Both ACE inhibitors were associated with an increase in the concentration of whole blood ANG I; however, tissue ANG I levels were significantly increased only following ACE inhibition with ramiprilat but not with enalaprilat. Both plasma and urinary bladder tissue ANG-(1-8) levels decreased significantly following ACE inhibition, but only with ramiprilat. The elevated urinary bladder tissue levels of ANG I and ANG-(1-8) at baseline, compared with circulating levels, and the maintenance of ANG-(1-8) in bladder tissue in the face of inhibition of the circulatory renin-angiotensin system with enalaprilat support the presence of an autocrine/paracrine renin-angiotensin system in the urinary bladder. Under the current experimental conditions, ramiprilat appears to have enhanced bladder activity compared with enalaprilat.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8840953&dopt=Abstract




Klin Med (Mosk). 2000;78(3):42-6.
[Effects of angiotensin-converting enzyme (ACE) inhibitors on water-salt homeostasis in hypertensive patients living in Far North]

[Article in Russian]

Vershinina AM, Gapon LI, Bazhukhina IF, Teffenberg DV, Drozdov VV, Spitsina NA, Sergeichik OI.

The aim of the study was evaluation of ACE inhibitors (captopril and ramipril) effect on water-salt homeostasis in the treatment of patients with arterial hypertension (AH) living in the Far North of Russia. 100 male patients with mild and moderate AH were examined 2 weeks, 3 and 6 months after administration of captopril or ramipril. The drugs are shown to correct water-salt metabolism. This is explained by better renal function due to speeding up glomerular filtration and increased sodium excretion with urine, and by activity of humoral mechanisms (inhibited activity of plasma renin, low plasma concentration of aldosterone and its 24-h excretion). Comparison of captopril versus ramipril demonstrates advantages of prolonged ramipril in respect to regulation of water salt metabolism in the treatment of essential hypertension in the Far North.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10790965&dopt=Abstract




Hypertension. 1992 Oct;20(4):478-82.
Effect of early onset angiotensin converting enzyme inhibition on myocardial capillaries.

Unger T, Mattfeldt T, Lamberty V, Bock P, Mall G, Linz W, Scholkens BA, Gohlke P.

Department of Pharmacology, University of Heidelberg, Frankfurt/Main, FRG.

We investigated the preventive effects of long-term treatment with the angiotensin converting enzyme inhibitor ramipril on myocardial left ventricular hypertrophy and capillary length density in spontaneously hypertensive rats. Rats were treated in utero and subsequently up to 20 weeks of age with a high dose (1 mg/kg per day) or with a low dose (0.01 mg/kg per day) of ramipril. Animals given a high dose of ramipril remained normotensive, whereas those given a low dose developed hypertension in parallel to vehicle-treated controls. At the end of the treatment period, converting enzyme activity in heart tissue was inhibited dose-dependently in the treated groups. Both groups revealed an increase in myocardial capillary length density together with increased myocardial glycogen and reduced citric acid concentrations. Left ventricular mass was reduced only in high dose- but not in low dose-treated animals. Our results demonstrate that early onset treatment with a converting enzyme inhibitor can induce myocardial capillary proliferation, even at doses too low to antagonize the development of hypertension or left ventricular hypertrophy. We hypothesize that potentiation of kinins is responsible for this effect, probably by augmenting myocardial blood flow, which is a well-known trigger mechanism of angiogenesis in the heart.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1328047&dopt=Abstract













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