Drugs online research references
Hypertension. 1990 Dec;16(6):662-8.
Regression of cardiac hypertrophy in spontaneously hypertensive rats by enalapril and the expression of contractile proteins.
Childs TJ, Adams MA, Mak AS.
Department of Biochemistry, Queen's University, Kingston, Ontario, Canada.
Several experimental models involving the development of cardiac hypertrophy in adult rats are characterized by the reexpression of the fetal isoform of myosin heavy chain (V3). To determine whether a similar adult-to-fetal shift in the expression of the thin-filament proteins occurs during cardiac hypertrophy, we have examined the expression of the isoforms of myosin, tropomyosin, and troponin T in the left ventricle of young spontaneously hypertensive rats (SHR) with and without treatment using enalapril, an angiotensin converting enzyme inhibitor. Phosphorylation of tropomyosin, which is predominant in the fetal state, was also analyzed. Twelve-week-old SHR were treated with enalapril for 2, 5, 8, and 9 weeks followed by withdrawal of treatment for 9 weeks. Control SHR, without drug treatment, were weight- and age-matched. After 9 weeks of enalapril treatment, mean arterial blood pressure was reduced (from 166 +/- 11 to 89 +/- 5 mm Hg), and left ventricular weight/body weight ratio was regressed (from 2.53 +/- 0.14 to 1.96 +/- 0.05 g/kg) to normotensive levels. During the 9-week treatment period, the percent V3 decreased in SHR substantially from 35 +/- 3% to 13 +/- 1%. There was a significant correlation between the left ventricular hypertrophy and the percent V3 myosin expression in the SHR during regression (r = 0.697, p less than 0.001). However, only the adult isoforms of tropomyosin and troponin T were detected in the SHR with or without enalapril treatment, and the level of tropomyosin phosphorylation remained constant irrespective of the degree of left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2147174&dopt=Abstract
J Cardiovasc Pharmacol. 1987;10 Suppl 6:S148-52.
Regression of cardiac hypertrophy: experimental and clinical results.
Motz W, Klepzig M, Strauer BE.
Department of Medicine, University of Dusseldorf, F.R.G.
Since left ventricular hypertrophy is considered to be a precursor of later hypertensive heart failure, a treatment that can prevent or even reverse myocardial hypertrophy is a highly desirable goal. In order to evaluate which type of antihypertensive treatment is able to induce regression of hypertensive hypertrophy, experimental and clinical studies were performed. Experimental studies were performed in spontaneously hypertensive rats (SHRs). Left ventricular hypertrophy and pumping function were studied after antihypertensive treatment with a beta-receptor blocker (metoprolol), an arteriolar vasodilator (hydralazine), and a calcium channel blocker (nifedipine) had been instituted for a period of 20-40 weeks. Patients with hemodynamically compensated hypertensive heart disease were treated with a calcium channel blocker (nifedipine), an angiotensin-converting enzyme (ACE) inhibitor (enalapril), an antisympathetic agent (clonidine), and prazosin. Comparing the amount of blood pressure reduction with the extent of hypertrophy reversal, nifedipine, prazosin, and enalapril were equipotent, whereas clonidine was most efficient in this respect. Muscle mass was overproportionally reduced in relation to blood pressure reduction following treatment with clonidine. It is likely that this was caused by lowered catecholamine levels secondary to clonidine therapy. Left ventricular pumping function was enhanced as a result of a reduction in left ventricular afterload, whereas myocardial contractility was found to be unchanged.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2485021&dopt=Abstract
Am J Nephrol. 1995;15(2):129-36.
Prevention of cardiac hypertrophy in experimental chronic renal failure by long-term ACE inhibitor administration: potential role of lysosomal proteinases.
Suzuki H, Schaefer L, Ling H, Schaefer RM, Dammrich J, Teschner M, Heidland A.
Department of Internal Medicine, University of Wurzburg, Germany.
The pathogenesis of cardiac hypertrophy in chronic uremia is poorly understood. In the present study, the long-term effects of chronic uremia on cardiac morphology and various cysteine proteinases of the heart were investigated in rats with and without antihypertensive therapy by the angiotensin converting enzyme inhibitor enalapril or by the calcium channel blocker verapamil. 16 weeks after subtotal nephrectomy considerable uremia had developed associated with arterial hypertension, rise in heart weight and heart weight/body weight ratio. Morphologically myocardial cells developed marked hypertrophy. Determination of various cysteine proteinases by fluorometry revealed a significant decline of cathepsin B activity while the activities of cathepsin H and L were unchanged. Antihypertensive treatment with enalapril and verapamil normalized the blood pressure and improved renal function significantly. Myocardial cell hypertrophy and the enhanced heart weight/body weight ratio were normalized under treatment with enalapril but not with verapamil. Simultaneously, the impaired cathepsin B activity returned to the normal range after enalapril treatment. It is concluded that the cardiac hypertrophy in uremia is at least partly caused by an activation of the circulating and/or cardiac renin-angiotensin system. Impaired proteinase activity in the uremic state may be involved in the development of cardiac hypertrophy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7733149&dopt=Abstract
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