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Am J Kidney Dis. 1988 Jun;11(6):499-507.
Effect of lisinopril monotherapy on renal hemodynamics.

Reams GP, Bauer JH.

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

Nineteen essential hypertensive patients were entered into a protocol to assess the BP, humoral and renal effects of the angiotensin converting enzyme inhibitor, lisinopril (MK 521, 20 to 80 mg once daily), administered for 52 weeks. Specifically monitored prior to, and following 12 and 52 weeks of lisinopril monotherapy were plasma renin activity and plasma aldosterone, the clearances of creatinine, inulin and para-aminohippurate, and the 24-hour urinary excretion of protein. BP was well controlled. Plasma renin activity was stimulated, and plasma aldosterone was suppressed throughout the entire protocol. In contrast to the reported short-term and long-term renal effects of enalapril, lisinopril (a lysine analog of enalapril) had no short-term effect on renal function: glomerular filtration rate, effective renal plasma flow, filtration fraction (FF), renal vascular resistance (RVR), and protein excretion were all unchanged. However, following long-term therapy, both FF and RVR were decreased. Lisinopril appears to convey no specific renal pharmacological benefit.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2837083&dopt=Abstract




Circulation. 1994 Jun;89(6):2852-9.
Effects of long-term monotherapy with enalapril, metoprolol, and digoxin on the progression of left ventricular dysfunction and dilation in dogs with reduced ejection fraction.

Sabbah HN, Shimoyama H, Kono T, Gupta RC, Sharov VG, Scicli G, Levine TB, Goldstein S.

Division of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, Detroit, Mich. 48202.

BACKGROUND: Recent clinical trials have suggested that therapy with angiotensin-converting enzyme inhibitors in asymptomatic patients with reduced left ventricular (LV) function can significantly reduce the incidence of congestive heart failure compared with patients receiving placebo. In the present study, we examined the effects of long-term monotherapy with enalapril, metoprolol, and digoxin on the progression of LV systolic dysfunction and LV chamber enlargement in dogs with reduced LV ejection fraction (EF). METHODS AND RESULTS: LV dysfunction was produced in 28 dogs by multiple sequential intracoronary microembolizations. Embolizations were discontinued when LVEF was 30% to 40%. Three weeks after the last embolization, dogs were randomized to 3 months of oral therapy with enalapril (10 mg twice daily, n = 7), metoprolol (25 mg twice daily, n = 7), digoxin (0.25 mg once daily, n = 7), or no treatment (control, n = 7). As expected, in untreated dogs, LVEF decreased (36 +/- 1% versus 26 +/- 1%, P < .001) and LV end-systolic volume (ESV) and end-diastolic volume (EDV) increased during the 3-month follow-up period (39 +/- 4 versus 57 +/- 6 mL, P < .001, and 61 +/- 6 versus 78 +/- 8 mL, P < .002, respectively). In dogs treated with enalapril or metoprolol, LVEF remained unchanged or increased after therapy compared with before therapy (35 +/- 1% versus 38 +/- 3% and 35 +/- 1% versus 40 +/- 3%, respectively, P < .05), whereas ESV and EDV remained essentially unchanged. In dogs treated with digoxin, EF remained unchanged but ESV and EDV increased significantly. CONCLUSIONS: In dogs with reduced LVEF, long-term therapy with enalapril or metoprolol prevents the progression of LV systolic dysfunction and LV chamber dilation. Therapy with digoxin maintains LV systolic function but does not prevent progressive LV enlargement.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8205701&dopt=Abstract




J Card Fail. 1997 Mar;3(1):53-61.
Electrophysiologic and morphologic abnormalities in the failing heart: effect of enalapril on the electrical properties.

De Mello WC, Cherry RC, Manivannan S.

Department of Pharmacology, School of Medicine, University of Puerto Rico, San Juan 00936-5067.

BACKGROUND: Knowledge of the electrophysiologic abnormalities in the failing heart is meager. In this work morphologic and electrophysiologic changes were investigated in the cardiomyopathic hamster (BIO TO-2) at 11 months of age. The results were compared with control hamsters (F1B) of the same age. METHODS AND RESULTS: Conventional KCl microelectrodes were used to measure membrane potential, conduction velocity, and refractoriness. Histologic studies consisted of Harris' hematoxylin and eosin, Masson trichrome, and von Kossa's calcium stain. The resting potential of myopathic fibers (-67.8 mV; SEM 1 0.83) in the cardiomyopathic hamsters was less negative than the control subjects' potential (-78.5 V; SEM + 1), and the action potential duration measured at 50% of repolarization was increased by 213%. The conduction velocity (36.9 cm/s) was 15.7% lower than that of the control subjects. Enalapril (50 micrograms/mL) caused a hyperpolarization of 6.8 mV, it increased the action potential duration at 90% of repolarization by 110%, and the conduction velocity of the myopathic fibers was appreciably increased compared to the control hamsters'. The refractoriness of myopathic and normal ventricular fibers was also increased by enalapril. Histologic studies performed on the right and left ventricular wall indicated interstitial fibrosis, necrotic foci, and extensive calcification. CONCLUSIONS: The results indicate severe morphologic and electrophysiologic abnormalities in the failing ventricular muscle. The effect of enalapril on membrane potential and conduction velocity might indicate that the activation of the cardiac renin-angiotensin system during the process of heart failure is, in part, responsible for the abnormalities described here. The improvement of impulse propagation and the increase in refractoriness seem to represent important factors involved in the antiarrhythmic action of enalapril.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9110255&dopt=Abstract












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