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Clin Exp Pharmacol Physiol. 1989 Apr;16(4):315-7.
Effect of enalapril on handling of a sodium chloride load by genetically hypertensive and normotensive rats.

Ledingham JM, Simpson FO.

Wellcome Medical Research Institute, University of Otago Medical School, Dunedin, New Zealand.

1. Enalapril was given in the drinking water (300 mg/L) for 4.5 days to normotensive (N) and genetically hypertensive (GH) rats on zero sodium intake. An intraperitoneal NaCl load was given 12 h after enalapril was started. 2. Enalapril did not increase the maximum rate of sodium excretion, but caused the rats to excrete more than the load in the first 24 h and then to have a slow fall in body sodium while on a sodium-free diet. 3. In terms of the Strauss et al. (1958) concept of body sodium, enalapril appears to lower the basal level. However, in addition it causes a slow leak of sodium which becomes apparent when sodium intake is very low.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2545395&dopt=Abstract




Clin Ther. 1987;9(6):635-9.
Increase in plasma HDL-cholesterol in hypertensive patients treated with enalapril.

Perani G, Muggia C, Martignoni A, Bongarzoni A, Radaelli A, Testa F, Finardi G.

Department of Internal Medicine, University of Pavia, Italy.

The effects of enalapril on plasma lipoproteins were evaluated in an open study of 12 normolipidemic outpatients with mild-to-moderate essential hypertension (World Health Organization stages I and II). After a two-week washout period, during which placebo was given, the patients received 20 to 40 mg/day of enalapril for 16 weeks. Treatment with enalapril was associated with significant increases in levels of HDL cholesterol (mean, 23%; P less than 0.001) and apoprotein A (mean, 11%; P less than 0.01), largely because of the increase in the subfraction HDL2 (mean, 43%; P less than 0.001), although the subfraction HDL3 also rose (mean, 14%; P less than 0.005). Total cholesterol and LDL cholesterol levels did not change, whereas triglycerides decreased significantly (mean, 26%; P less than 0.001). Apoprotein B was unchanged. Unlike diuretics and most beta-blockers, enalapril favorably affects plasma lipoprotein levels, thus improving the overall cardiovascular risk in hypertensive patients.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2830973&dopt=Abstract




Zhonghua Yi Xue Za Zhi (Taipei). 1991 Jul;48(1):31-40.
Enalapril in congestive heart failure: acute hemodynamic and neurohumoral evaluation and short-term follow-up.

Lin M, Chiang HT, Chang MS, Kong CW, Wang SP, Chiang BN.

Department of Internal Medicine, National Yang-Ming Medical College, Taipei, R.O.C.

The acute efficacy of rapid loading of oral long-acting enalapril in congestive heart failure remains to be established. We evaluated the efficacy of this treatment modality in 22 patients with chronic congestive heart failure N.Y.H.A. functional class ranging from II-IV with Creatinine level less than 2 mg/dl. Following hemodynamic evaluation, there was significant favorable change in the left ventricular functional curve. Moreover, acute hemodynamic assessment showed a significant reduction in pulmonary capillary wedge pressure from 19.2 +/- 4.8 to 17.2 +/- 4.7 mmHg (p less than 0.005) and an increases in stroke volume index from 28.3 +/- 9.2 to 33.1 +/- 7.5 ml/m (p less than 0.005). After rapid enalaprilization, blood pressure fell from 127 +/- 21/78 +/- 15 to 108 +/- 21/68 +/- 15 mmHg (p less than 0.005), systemic vascular resistance from 1725 +/- 602 to 1370 +/- 376 dyne.sec.cm-5 (p less than 0.05) and pulmonary vascular resistance from 262 +/- 19 to 218 +/- 65 dyne.sec.cm-5 (p less than 0.05). Cardiac index rose significantly from 2.43 +/- 0.62 to 2.60 +/- 0.50 l/min/m2 (p less than 0.05). In terms of neurohumoral assessments, there was a significant inhibition of the renin-angiotensin-aldosterone system. Aldosterone fell from 21.3 +/- 13.4 to 9.4 +/- 8.0 ng/dl and plasma renin activity rose from 3.3 +/- 4.6 to 11.3 +/- 11.0 ng/nl/hr (p less than 0.005). Plasma norepinephrine and epinephrine levels were found to have significant reduction in addition to antidiuretic hormone concentration. During short-term trial, left ventricular ejection fraction was significantly elevated from 27.5 +/- 6% to 32.8 +/- 10.8% (p less than 0.005). Thus, this limited study clearly demonstrates the rapid administration of enalapril not only achieves inhibition of renin-angiotensin-aldosterone system but also reduces preload and afterload significantly in the failing heart. We conclude that rapid enalaprilization is an effective methodology which still needs meticulous attention, providing significant hemodynamic and symptomatic benefits in patients with chronic congestive heart failure.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1679372&dopt=Abstract












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