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Captopril: pharmacokinetics, antihypertensive and biological effects in hypertensive patients.
Author(s) -
Richer C,
Giroux B,
Plouin PF,
Maarek B,
Giudicelli JF
Publication year - 1984
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1984.tb02338.x
Subject(s) - captopril , cmax , pharmacokinetics , pharmacology , bioavailability , blood pressure , plasma renin activity , chemistry , oral administration , essential hypertension , endocrinology , medicine , renin–angiotensin system
The kinetics of captopril plasma levels and of the drug‐induced plasma converting enzyme activity (PCEA), plasma renin activity (PRA) and diastolic blood pressure (DBP) modifications were studied over 24 h after oral administration of captopril, 1 mg/kg, to ten hypertensive patients. Free unchanged captopril pharmacokinetic parameters were: t1/2, alpha: 0.45 +/‐ 0.06 h; tmax: 0.98 +/‐ 0.13 h; Cmax: 1.31 +/‐ 0.20 mg l‐1; t1/2,z: 0.66 +/‐ 0.13 h; V: 0.614 +/‐ 0.104 1 kg‐1 and CLtot: 0.690 +/‐ 0.082 l h‐1 kg‐1. At 6 h captopril was no longer detectable in plasma. The onset of PCEA inhibition and of DBP decrease closely followed the rise of captopril's plasma levels, while that of PRA increase was delayed. In contrast, while captopril rapidly disappeared from plasma, its biological and antihypertensive effects were long‐lasting. The lack of correlation between the relative bioavailability of captopril and the induced reduction in DBP (evaluated by the corresponding AUCs) suggests that free unchanged captopril plasma monitoring is not an adequate indicator of hypertensive patients' potential responsiveness to captopril's blood pressure lowering effects.