Drugs online research references
J Am Coll Cardiol. 2000 Jul;36(1):276-81.
Effect of carvedilol in comparison with metoprolol on myocardial collagen postinfarction.
Wei S, Chow LT, Sanderson JE.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, SAR.
OBJECTIVES: We sought to compare the effects of two different beta-blockers, carvedilol and metoprolol, to an angiotensin-converting enzyme (ACE) inhibitor (captopril) on myocardial collagen deposition during healing and ventricular remodeling after myocardial infarction (MI). BACKGROUND: Beta-adrenergic blockade has been shown to be beneficial post-MI and in chronic heart failure. Carvedilol is a new-generation vasodilating beta-blocker with additional alpha1-adrenoceptor antagonism and an antiproliferative action, but it is not known if it is more beneficial than standard selective beta-blockers. METHODS: Using a rat model of MI, induced by left coronary ligation, we studied the effects of 11 weeks of therapy with oral carvedilol, metoprolol or captopril on hemodynamics, tissue weights, collagen volume fraction and hydroxyproline content. RESULTS: Both beta-blockers caused similar decreases in heart rate and LVEDP compared with untreated post-MI rats. At equivalent beta-adrenoceptor blocking doses, however, carvedilol, but not metoprolol, attenuated the increase in collagen content in noninfarcted regions and prevented the increase in right ventricular weight/body weight (all p < 0.05), and its effect was similar to captopril. Metoprolol treatment tended to increase right ventricular weight and heart weight (p < 0.05). There were no differences in infarct size between the groups. CONCLUSIONS: Long-term treatment with both beta-blockers, as well as an ACE inhibitor, benefited the healing process in rats post-MI. At equivalent myocardial beta-adrenoceptor blocking doses, however, carvedilol significantly reduced myocardial collagen in the noninfarcted myocardium and cardiac hypertrophy in the right ventricle, whereas metoprolol had no effect on myocardial collagen deposition.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10898446&dopt=Abstract
Am J Physiol Heart Circ Physiol. 2000 Jul;279(1):H269-78.
Reinforcement of arteriolar myogenic activity by endogenous ANG II: susceptibility to dietary salt.
Nurkiewicz TR, Boegehold MA.
Department of Physiology, West Virginia University School of Medicine, Morgantown, West Virginia 26505-9229, USA.
The purpose of this study was to determine whether endogenous ANG II augments arteriolar myogenic behavior in striated muscle. Because circulating ANG II is decreased during high salt intake, we also investigated whether dietary salt could alter any influence of ANG II on myogenic behavior. Normotensive rats fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated box with the spinotrapezius muscle exteriorized for intravital microscopy. Dietary salt did not affect resting arteriolar diameters. Microvascular pressure elevation by box pressurization caused greater arteriolar constriction in LS rats (up to 12 microm) than in HS rats (up to 4 microm). The ANG II-receptor antagonists saralasin and losartan attenuated myogenic responsiveness in LS rats but not HS rats. The bradykinin-receptor antagonist HOE-140 had no effect on myogenic responsiveness in LS rats but augmented myogenic responsiveness in HS rats. HOE-140 with the angiotensin-converting enzyme inhibitor captopril attenuated myogenic responsiveness to a greater extent in LS rats than in HS rats. We conclude that endogenous ANG II normally reinforces arteriolar myogenic behavior in striated muscle and that attenuated myogenic behavior associated with high salt intake is due to decreased circulating ANG II and increased local kinin levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10899066&dopt=Abstract
Am J Respir Crit Care Med. 2000 Jul;162(1):310-5.
Targeting the angiotensin system in posttransplant airway obliteration: the antifibrotic effect of angiotensin converting enzyme inhibition.
Maclean AA, Liu M, Fischer S, Suga M, Keshavjee S.
Thoracic Surgery Research Laboratory, The Toronto General Hospital Research Institute, University of Toronto, Toronto, Ontario, Canada.
The angiotensin system plays a role in the pathogenesis of fibrotic diseases. We used a rat heterotopic tracheal transplant model of bronchiolitis obliterans (BO) to examine the role of angiotensin converting enzyme (ACE) in development of the fibroproliferative lesion of BO. Isograft and allograft tracheal transplants were performed. Allograft rats received either no treatment (control) or captopril (100 mg/kg/d) in their drinking water. The drug treatment given to the recipient rats was begun 5 days before transplantation, on postoperative Day 1, or on postoperative Day 5. The treatment was continued until postoperative Day 21, when tracheal specimens were harvested and subjected to histologic, immunohistologic, and morphometric analyses. We noted heavy staining for ACE in the obliterated portion of the tracheas of allograft control animals. This area was not present in nontransplanted or isograft tracheas. Captopril administration begun 5 d before transplantation and on postoperative Day 1 resulted in a significant attenuation in the percent airway obliteration (45% and 26%, respectively) as compared with that in control allografts (83%; p < 0.05). This study demonstrates the presence of ACE in the fibroproliferative lesion in a rat model of BO, and shows that inhibition of ACE can limit development of airway obliteration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10903259&dopt=Abstract
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