The Clinical Pharmacokinetics of Quinapril

Horvath, Ann Marie; Michniewicz, Barbara M.; Sedman, Allen J.; Colburn, Wayne A.; Welling, Peter G.; Olson, Stephen C.

doi:10.1177/000331978904000404

Cited by 84 publications

(25 citation statements)

References 21 publications

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“…After a dose of 2.5 mg p.o. in healthy subjects, the Cmax was 41 (12.7) (SD) ng/ml [1]. In our study mean Cm~x ranged from 63.3 (CAPD patients) to 83.5 ng.…”

Section: Discussionsupporting

confidence: 41%

“…The peak plasma concentration of quinaprilat occurred later (4 to 4.7 h) than in healthy subjects (2 h), independent of dose [1]. The tmax reported in CAPD patients after 20 mg was 5.4 (2.5) (SD) h [4] and 4.5 (2.5) (SD) h in chronic HD patients [3].…”

Section: Discussionmentioning

confidence: 88%

“…Apparent elimination half life (t1/2) was calculated as ln2/)~z. Apparent total clearance was estimated by multiplying the applied dose by the absorption factor (0.6) [1], and by dividing this dose by the AUC (0~). The peritoneal clearance of quinaprilat (CLp) was calculated from the cumulative 24 h excretion of quinaprilat in dialysate (CDE (gg)), where CLp = CDE/AUC (0-24) h).…”

Section: Pharmacokinetic Analysismentioning

confidence: 99%

“…At least 60 % of an oral dose of quinapril is rapidly absorbed in healthy volunteers, with a peak plasma concentration within i h, while plasma quinaprilat concentrations peak within 2 h [1]. Quinapril and quinaprilat are eliminated from plasma with apparent half lives of 0.8 and 1.9 h. A small amount of quinapril (3 %) is excreted in the urine, whereas 30 % of a dose is excreted as quinaprilat [1]. The elimination half life is prolonged in patients with impaired renal function [2].…”

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confidence: 99%

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Pharmacokinetics and pharmacodynamics of quinaprilat after low dose quinapril in patients with terminal renal failure

Wolter

Fritschka

1993

Eur J Clin Pharmacol

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The pharmacokinetics and pharmacodynamics of the ACE inhibitor quinaprilat have been studied in six chronic haemodialysis (HD) patients and in six patients undergoing continuous ambulatory peritoneal dialysis (CAPD) after a single oral dose of 2.5 mg quinapril. Mean tmax and Cmax values (SEM) for quinaprilat in interdialytic HD patients were 4.0 (0) h and 84 (8.4) ng.ml-1 respectively, and they did not differ significantly from those in CAPD patients (4.7 (0.7) h and 64 (5.7) ng.ml-1). Elimination half lives were 30 (10.1) h (HD) and 34 (7.3) h (CAPD). Cmax, tmax, t1/2, and AUC were increased and CL was decreased compared to data reported previously after giving 2.5 mg to healthy subjects. Peritoneal clearance was calculated as 0.1 (0.1) ml.min-1, thus less than 0.5% of the dose were removed within 24 h by CAPD. ACE activity was suppressed by more than 93% between 4 and 24 h postdose (P < 0.001). It decreased in both groups with increasing plasma quinaprilat levels. Angiotensin II concentration compared to baseline was significantly decreased at 4 hours (-30.4 +/- 10%) and 24 h (-30 +/- 9.9%) (P < 0.05, n = 11), while active plasma renin concentration was still significantly increased at 48 h postdose (+ 60.2 +/- 14.5%, P < 0.01). Mean arterial pressure 24 h postdose was significantly (P < 0.05) decreased in HD (-12 mmHg) and CAPD patients (-20 mm Hg). Only two patients reported unwanted effects (fatigue, dizziness, nausea, and weakness). In conclusion, due to its long lasting effect on ACE activity and on blood pressure in terminal renal failure a starting dose of quinapril 2.5 mg o.d. may be used in hypertensive HD and CAPD patients.

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“…After a dose of 2.5 mg p.o. in healthy subjects, the Cmax was 41 (12.7) (SD) ng/ml [1]. In our study mean Cm~x ranged from 63.3 (CAPD patients) to 83.5 ng.…”

Section: Discussionsupporting

confidence: 41%

Section: Discussionmentioning

confidence: 88%

Section: Pharmacokinetic Analysismentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Pharmacokinetics and pharmacodynamics of quinaprilat after low dose quinapril in patients with terminal renal failure

Wolter

Fritschka

1993

Eur J Clin Pharmacol

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“…l 3 The investigators reported that the HDWLDL cholesterol ratio remained virtually unchanged after 1 year of therapy with quinapril. Serum triglycerides did not increase.…”

Section: Plasma Lipid and Lipoprotein Levelsmentioning

confidence: 99%

Quinapril: Overview of preclinical data

Kaplan¹,

Taylor²,

Olson³

2009

Clin Cardiol

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Summary:Quinapril hydrochloride, a new, orally active, nonpeptide, nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor, has been studied extensively in a variety of in vitro and in vivo animal models. Quinapril inhibits the contractile and pressor effects of angiotensin I in rabbit aorta and in rats, respectively, and lowers blood pressure in both high-and normal-renin rodent and diuretic-treated dog models of hypertension. No tolerance to the antihypertensive effects of quinapril was noted in spontaneously hypertensive rats treated with quinapril for up to 14 consecutive days. As with other ACE inhibitors, quinapril had virtually no effect on the development of hypertension in the renin-independent one-kidney deoxycorticosterone (D0CA)-salt hypertensive rat. Antihypertensive activity best correlates with the inhibition of tissue (vascular) ACE, and thus the reduction in peripheral vascular resistance associated with plasma and tissue ACE most likely accounts for the therapeutic benefit of quinapril. Preliminary data from a trial of quinapril in cardiomyopathic hamsters show that the drug prevents the anticipated decline in left ventricular contractile function and retards the temporal progression of left ventricular failure. ACE inhibitors have been found to have a lipidneutral profile, unlike some other classes of antihypertensives. Quinapril is rapidly absorbed and extensively distributed to all tissues except brain. It is rapidly hydrolyzed to quinaprilat, its pharmacologically active diacid form. Metabolism to other compounds is not extensive. Quinapril's preclinical toxicologic profile is similar to that of other ACE inhibitors. Long-term toxicology studies show that quinapril is not teratogenic, carcinogenic, or mutagenic.

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Multiple‐dose propranolol administration does not influence the single dose pharmacokinetics of quinapril and its active metabolite (quinaprilat)

Horvath¹,

Pilon

Caillé

et al. 1990

Biopharm & Drug Disp

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To evaluate the influence of multiple dose propranolol administration on the single dose pharmacokinetics of quinapril and its active metabolite, quinaprilat, a drug-drug interaction study was performed in ten healthy volunteers. Each subject received a single 20 mg quinapril oral dose on Days 1 and 16 of the study. Oral propranolol doses of 40 mg BID were initiated on Day 3, titrated gradually to 80 mg TID by Day 10, and continued at 80 mg TID through Day 17. Comparable mean quinapril pharmacokinetic parameter values as well as comparable mean quinaprilat pharmacokinetic parameter values determined following quinapril administered alone and following quinapril administered with propranolol, indicate that propranolol does not alter the single dose pharmacokinetics of quinapril or quinaprilat.

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The Clinical Pharmacokinetics of Quinapril

Cited by 84 publications

References 21 publications

Pharmacokinetics and pharmacodynamics of quinaprilat after low dose quinapril in patients with terminal renal failure

Pharmacokinetics and pharmacodynamics of quinaprilat after low dose quinapril in patients with terminal renal failure

Quinapril: Overview of preclinical data

Multiple‐dose propranolol administration does not influence the single dose pharmacokinetics of quinapril and its active metabolite (quinaprilat)

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