Pharmacokinetic properties of captopril after acute and chronic administration to hypertensive subjects

Jarrott, Bevyn; Drummer, Olaf H.; Hooper, Rita; Anderson, Adrianne; Miach, P. J.; Louis, William J.

doi:10.1016/0002-9149(82)90385-x

Cited by 41 publications

(18 citation statements)

References 7 publications

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“…16) Oral administration study of prodrug-type ACE inhibitor, imidapril, to healthy human, 17) on the other hand, demonstrated that the plasma concentration reached a maximal level (C max at 10 mg-dose) of 70 pmol/ml-plasma after 2 h (T max ; 2 h). While the absorption profile of imidapril with T max of 2 h was in good agreement with that in our present VY-study (Fig.…”

Section: Resultsmentioning

confidence: 99%

Absorption of Val-Tyr with in Vitro Angiotensin I-Converting Enzyme Inhibitory Activity into the Circulating Blood System of Mild Hypertensive Subjects.

Matsui

Tamaya

Seki³

et al. 2002

Biological & Pharmaceutical Bulletin

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Section: Resultsmentioning

confidence: 99%

Absorption of Val-Tyr with in Vitro Angiotensin I-Converting Enzyme Inhibitory Activity into the Circulating Blood System of Mild Hypertensive Subjects.

Matsui

Tamaya

Seki³

et al. 2002

Biological & Pharmaceutical Bulletin

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“…0.110, NS) (b) PCEA% inhibition (r = 0.207, NS) and (c) the increase in PRA (r = 0.257, NS) and there was no correlation between PCEA% Discussion inhibition and (a) the decrease in DBP (r = 0.226, NS) and (b) the increase in PRA (r = Since appropriate methods for plasma captopril 0.491, NS), all these parameters being quantified monitoring have only recently become available, viously reported in normal subjects (tmaX = 0.7-0.9 h; t½,z = 0.35-1.7 h) (Kripalani et al, 1980;Onoyama et al, 1981;Duchin et al, 1982) or in hypertensive patients (tmax = 0.6-0.9 h; t,12, = 0.6-1.6 h) (Jarrott et al, 1981(Jarrott et al, , 1982 whatever the one- (Onoyama et al, 1981) or two-compartment (Duchin et al, 1982) pharmacokinetic model used. Captopril absorption is rapid since its half-life was 0.45 h and since after 20 min mean plasma levels were already 40% of their maximal values which were reached within 60 min.…”

Section: Correlationsmentioning

confidence: 99%

Captopril: pharmacokinetics, antihypertensive and biological effects in hypertensive patients.

Richer¹,

Giroux²,

Plouin³

et al. 1984

Brit J Clinical Pharma

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1 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. 3 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. 4 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.

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“…(Kripalani et al, 1980;Onoyama et al, 1981;Duchin et al, 1982) or in hypertensive subjects (tmax: 0.6-0.9 h; T½/2: 0.6-1.6 h) (Jarrott et al, 1981(Jarrott et al, , 1982Richer et al, 1984) whatever the one- (Onoyama et al, 1981;Richer et al, 1984) or two-compartment (Duchin et al, 1982) (Duchin et al, 1982) but at concentrations below its plasma detection threshold. Hence, these metabolites could in case of accumulation prolong the duration of captopril biological and clinical effects.…”

Section: Pcea Blockadementioning

confidence: 99%

Influence of chronic renal failure on captopril pharmacokinetics and clinical and biological effects in hypertensive patients.

Jf¹,

Chaignon²,

Richer³

et al. 1984

Brit J Clinical Pharma

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The pharmacokinetic parameters of unchanged plasma captopril and the kinetics of the drug effects on plasma converting enzyme activity (PCEA), plasma renin activity (PRA), plasma aldosterone (PA) and mean blood pressure (MBP) were studied over 24 h after oral administration in three groups of hypertensive patients: with normal renal function (group 1, plasma creatinine less than 110 mumol/l, n = 10), with moderate chronic renal failure (group 2, 135 less than plasma creatinine less than 450 mumol/l, n = 10) and with severe chronic renal failure (group 3, plasma creatinine greater than 500 mumol/l, n = 10). Renal impairment had no effect on plasma captopril Cmax, CLtot and relative bioavailability (AUC). In contrast, captopril kel decreased while T1/2 increased progressively from group 1 to group 3. PCEA blockade (T1/2 and AUC) was increased significantly and proportionally to the degree of renal impairment. However, there were no differences between the three groups regarding captopril‐induced modifications of PRA and PA. Although the maximal reduction in MBP was identical in the three groups, the overall antihypertensive effect (AUC) of captopril increased significantly and progressively from group 1 to group 3, especially in duration. There was no correlation between basal plasma creatinine values and unchanged captopril relative bioavailability (AUC) and between unchanged captopril relative bioavailability (AUC) and the drug effects (AUC) on PCEA, PRA, PA and MBP. However there was a correlation between basal plasma creatinine values and plasma captopril T1/2, PCEA blockade (AUC) and overall antihypertensive effect (AUC). The apparent discrepancy between the lack of effects of chronic renal failure on plasma unchanged captopril bioavailability and its potentiating effects on PCEA blockade and MBP reduction may be accounted for by the renal impairment‐induced accumulation of captopril metabolites.

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Pharmacokinetic properties of captopril after acute and chronic administration to hypertensive subjects

Cited by 41 publications

References 7 publications

Absorption of Val-Tyr with in Vitro Angiotensin I-Converting Enzyme Inhibitory Activity into the Circulating Blood System of Mild Hypertensive Subjects.

Absorption of Val-Tyr with in Vitro Angiotensin I-Converting Enzyme Inhibitory Activity into the Circulating Blood System of Mild Hypertensive Subjects.

Captopril: pharmacokinetics, antihypertensive and biological effects in hypertensive patients.

Influence of chronic renal failure on captopril pharmacokinetics and clinical and biological effects in hypertensive patients.

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