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Role of angiotensin II type 2 receptor during regression of cardiac hypertrophy in spontaneously hypertensive rats.
J Am Soc Hypertens
September 2013
Department of Pharmacology, Université de Montréal, Montreal, Quebec, Canada.
We previously reported that the AT1 receptor antagonist valsartan and the angiotensin converting enzyme (ACE) inhibitor enalapril decrease DNA synthesis and stimulate apoptosis in interstitial fibroblasts and epicardial mesothelial cells during regression of ventricular hypertrophy in spontaneously hypertensive rats (SHR). To examine the role of the AT2 receptor in this model, we studied hearts from SHR treated with valsartan or enalapril either alone or combined with the AT2 antagonist PD123319 for 1 or 2 weeks. Apoptosis was evaluated by quantification of DNA fragmentation or by TUNEL labeling.
View Article and Find Full Text PDFSynergistic interaction between enalapril, L-arginine and tetrahydrobiopterin in smooth muscle cell apoptosis and aortic remodeling induction in SHR.
Br J Pharmacol
July 2004
Department of Pharmacology, University of Montreal, University of Montreal Hospital (CHUM) Research Center, 3840 St. Urbain St., Room 7-132B, Montreal, Quebec, Canada H2W 1T8.
Smooth muscle cell (SMC) apoptosis occurs at the onset of enalapril-induced regression of aortic hypertrophy in SHR. A potential mechanism is the correction of endothelial dysfunction (ED) leading to reduced production of reactive oxygen species and enhanced bioavailability of nitric oxide (NO), a potent apoptosis inducer. Stimulants of NO include the precursor L-arginine and the NO synthase cofactor tetrahydrobiopterin (BH(4)), which correct ED in several models.
View Article and Find Full Text PDFKinin B2 receptor is not involved in enalapril-induced apoptosis and regression of hypertrophy in spontaneously hypertensive rat aorta: possible role of B1 receptor.
Br J Pharmacol
February 2004
Department of Pharmacology, Université de Montreal Hospital (CHUM) Research Center 3840, St-Urbain St., Room 7-132B, Montréal, PQ, Canada, H2W 1T8.
1. Treatment with enalapril induces smooth muscle cell apoptosis and regression of aortic hypertrophy in spontaneously hypertensive rats (SHRs), whereas combined blockade of angiotensin II AT(1) and AT(2) receptors does not. We postulated that vascular apoptosis with enalapril involves enhanced half-life of bradykinin (BK) and kinin B(2) receptor stimulation.
View Article and Find Full Text PDFProapoptotic and growth-inhibitory role of angiotensin II type 2 receptor in vascular smooth muscle cells of spontaneously hypertensive rats in vivo.
Hypertension
May 2000
Centre de Recherche, Centre Hospitaliér de l'Université de Montréal (CHUM), Montreal, Quebec, Canada.
Angiotensin type 2 (AT(2)) receptors for angiotensin II suppress cell growth and induce apoptosis in vitro, but their role is poorly defined in vivo. We reported that transient induction of smooth muscle cell (SMC) apoptosis precedes DNA synthesis inhibition and aortic hypertrophy regression in spontaneously hypertensive rats treated with the AT(1) antagonist losartan or the converting-enzyme inhibitor enalapril. Although both drugs are equipotent in reducing SMC number, apoptosis occurs significantly earlier with losartan than enalapril.
View Article and Find Full Text PDFEnalapril induces regression of cardiac hypertrophy and normalization of pHi regulatory mechanisms.
Hypertension
April 1998
Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Argentina.
Intracellular pH is under strict control in myocardium; H+ are extruded from the cells by sodium-dependent mechanisms, mainly Na+/H+ exchanger and Na+/HCO3- symport, whereas Na+-independent Cl-/HCO3- exchanger extrudes bases on intracellular alkalinization. Hypertrophic myocardium from spontaneously hypertensive rats (SHR) exhibits increased Na+/H+ exchange activity that is accompanied by enhanced extrusion of bases through Na+-independent Cl-/HCO3- exchange. The present experiments were designed to investigate the effect of enalapril-induced regression of cardiac hypertrophy on the activity of these exchangers.
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