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Int J Clin Pharmacol Ther Toxicol. 1987 Dec;25(12):656-9.
Systemic and renal hemodynamic changes after two-month treatment with enalapril in patients with essential hypertension.

Valvo E, Gammaro L, Bedogna V, Tonon M, Giorgetti P, Pica B, Antonini P, Tessitore N, Oldrizzi L, Rugiu C, et al.

Department of Nephrology, University Hospital of Verona, Italy.

Twelve essential hypertensive patients with normal renal function were treated once daily with a new angiotensin converting enzyme inhibitor, enalapril maleate, for about two months. In all patients, the drug-induced changes in blood pressure (BP), systemic and renal hemodynamics, plasma renin activity (PRA), and urine aldosterone (UA) were evaluated. Mean arterial pressure was significantly lowered. No significant changes in cardiac index, heart rate, and stroke index were observed, while peripheral vascular resistance index was significantly decreased. Plasma and blood volumes were not significantly altered. The effects on renal hemodynamics consisted of a significant increase in renal plasma flow (RPF), a decrease in renal vascular resistance, and no change in glomerular filtration rate (GFR). UA excretion was significantly reduced during enalapril therapy. The drug was well tolerated, and no side effects were observed. In summary, enalapril is able to reduce blood pressure through a vasodilatatory effect without change in cardiac output. It increases renal blood flow with no change in glomerular filtration rate.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2830196&dopt=Abstract




Clin Exp Hypertens A. 1987;9(2-3):297-306.
Acute and subacute hemodynamic effects of enalaprilat, milrinone and combination therapy in rats with chronic left ventricular dysfunction.

Emmert SE, Stabilito II, Sweet CS.

A model of congestive heart failure (CHF) was produced in rats approximately 76 days following surgical occlusion of the left coronary artery. In rats with healed myocardial infarction (MI size = 45% LV), hemodynamic variables were predictably elevated (LVEDP greater than 20 mm Hg) or depressed LV dP/dtmax (5200 mm Hg/sec). The hemodynamic response (MAP, HR, LVEDP, and dP/dtmax) to intravenous infusion of Mil (54 to 347 micrograms/kg) was measured on two occasions, separated by a 7-12 day period of oral treatment (2 mg/kg/day). Enalaprilat was tested in a similar design with the infusion phase (70 micrograms/kg, total dose) separated by oral enalapril (Enal), 1 mg/kg/day. The hemodynamic response to Mil was also examined in rats treated with the ACE inhibitor. At low doses, Mil modestly elevated HR (+17 beats/min) and dose-dependently increased (P less than 0.05) LV contractility by approximately 25%. Higher doses of Mil reduced preload (LVEDP) and afterload (MAP). Oral Mil produced little hemodynamic improvement except modest elevation (+9%) in LV contractility. There was no evidence of tachyphylaxis to i.v. Mil. In contrast, enalaprilat reduced MAP and preload without altering HR or contractility, effects observed after oral treatment. In the presence of the ACE inhibitor, Mil's hemodynamic actions were not enhanced. These experiments demonstrate that ACE inhibition improves ventricular performance by reducing preload and afterload. In this model, Mil improves performance by a direct inotropic mechanism as well as a reduction in afterload.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3038390&dopt=Abstract




Kardiol Pol. 1992 Jul;37(7):3-7.
[Enalapril improves hemodynamics and exercise tolerance in pulmonary heart disease caused by obstructive lung disease]

[Article in Polish]

Lewczuk J, Wrabec K, Piszko P, Jagas J, Porada A, Reczuch K, Spikowski J.

Oddzialu Internistyczno-Kardiologicznego Wojewodzkiego Szpitala Specjalistycznego we Wroclawiu.

Chronic enalapril therapy was assessed in 11 patients with cor pulmonale due to chronic obstructive pulmonary disease. Enalapril was added to the maintenance dose of diuretics and digitalis and when clinical stabilisation was achieved haemodynamics, spirometry, blood gases and maximal treadmill exercise test accompanied by +pulse oximetry were performed before and after 30 days, 10-20 mg a day, enalapril therapy. Haemodynamic study showed moderate but significant decrease in mean pulmonary artery pressure, from 24 +/- 3 to 21 +/- 5 mmHg (p = 0.05). There were no substantial differences in cardiac output as well as in blood gases and spirometry after enalapril therapy. Slight decrease in oxygen delivery, on an average from 9157 +/- 3808 to 8074 +/- 3574 (p = NS), was accompanied by a concomitant fall in haemoglobin. We noted significant improvement of maximal exercise test results after enalapril therapy. Maximal workload achieved and the time of exercise increased. It was accompanied by subjective improvement as assessed by Borg scale. We observed no adverse effects of enalapril during one month therapy in patients with cor pulmonale and COPD.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1405196&dopt=Abstract













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