
Effects of the Converting Enzyme Inhibitor Quinapril (CI-906) on Blood Pressure, Renin-Angiotensin System, and Prostanoids in Essential Hypertension
Author(s) -
P Säynävälammi,
Ilkka Pörsti,
P Pörsti,
Anna-Kaisa Nurmi,
Erkki Seppälä,
Vesa Manninen,
Heikki Vapaatalo
Publication year - 1988
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-198807000-00012
Subject(s) - quinapril , endocrinology , angiotensin converting enzyme , medicine , blood pressure , angiotensin ii , plasma renin activity , essential hypertension , placebo , metabolite , chemistry , renin–angiotensin system , thromboxane , thromboxane b2 , ace inhibitor , platelet , alternative medicine , pathology
Fourteen patients with mild to moderate essential hypertension were randomized, after a baseline placebo period of 4 weeks, to receive the angiotensin converting enzyme (ACE) inhibitor quinapril or a placebo. During a 12 week, double-blind phase, the dosage of quinapril was increased from 10 to 40 mg twice daily being doubled every 4 weeks. At the end of the baseline period and of each month of the double-blind phase, 12 h overnight urine collections were made and morning blood samples were taken about 12 h after the last dose of medication. During the double-blind phase, blood pressure in the quinapril group (n = 7) decreased from 159 +/- 3/105 +/- 1 to 141 +/- 6/94 +/- 2 mm Hg (mean +/- SEM). Serum ACE activity and plasma angiotensin II concentration were reduced to 4 +/- 1% and 14 +/- 1% of the pretreatment values, respectively. Neither the plasma concentrations nor the urinary excretions of prostaglandin E2, 6-keto-prostaglandin F1 alpha (a prostacyclin metabolite), or thromboxane B2 (a metabolite of thromboxane A2) were affected by quinapril. In the placebo group, blood pressure tended to decline but the biochemical variables remained essentially unchanged. These results indicate that prostanoids are not involved in the antihypertensive action of quinapril, the principal effect of which seems to be inhibition of the renin-angiotensin system.