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In hemodynamic studies in patients with essential hypertension, blood pressure reduction was accom-panied by a reduction in peripheral arterial resistance with little or no change in cardiac output and in heart rate. In a study in nine hypertensive patients, following administration of PRINIVIL ® , there was an increase in mean renal blood flow that was not significant. Data from several small studies are inconsistent with respect to the effect of PRINIVIL ® on glomerular filtration rate in hypertensive patients with normal renal function, but suggest that changes, if any, are not large. When PRINIVIL ® is given together with thiazide-type diuretics, its blood pressure lowering effect is approximately additive. The antihypertensive effect of angiotensin converting enzyme inhibitors is generally lower in black than in non-black patients. Text Continues Below
Administration of PRINIVIL ® to patients with congestive heart failure reduces afterload and preload of the heart, resulting in an increase in cardiac output, without reflex tachycardia. Exercise tolerance is improved. Pharmacokinetics After oral administration of PRINIVIL ® , peak serum concentrations of lisinopril occur within approximately 7 hours, although patients with recent myocardial infarction have demonstrated an increase in time to peak serum concentration to about 8 to 10 hours. Declining serum concentrations exhibit a prolonged terminal phase which does not contribute to drug accumulation. This terminal phase probably represents saturable binding to ACE and is not proportional to dose. Lisinopril does not bind serum proteins other than ACE. Lisinopril does not undergo metabolism and is excreted unchanged entirely in the urine. Based on urinary recovery, the extent of absorption of lisinopril is approximately 25%, with large inter-subject variability (6Ð 60%) at all doses tested (5-80 mg). Lisinopril absorption is not influenced by the presence of food in the gastrointestinal tract. Page: << Prev | 1 | 2 | 3 | Next >>
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