![]() ![]() Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of fosinopril sodium remains to be elucidated. Removal of angiotensin II negative feedback on renin secretion leads to increased plasma renin activity.ĪCE is identical to kininase, an enzyme that degrades bradykinin. Similar increases were observed among all patients treated with fosinopril, including those receiving concomitant diuretic therapy. In 647 hypertensive patients treated with fosinopril alone for an average of 29 weeks, mean increases in serum potassium of 0.1 mEq/L were observed. The latter decrease may result in a small increase of serum potassium. Inhibition of ACE results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decreased aldosterone secretion. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. In animals and humans, fosinopril sodium is hydrolyzed by esterases to the pharmacologically active form, fosinoprilat, a specific competitive inhibitor of angiotensin-converting enzyme (ACE).ĪCE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin l to the vasoconstrictor substance, angiotensin II. ![]()
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