Prolonged converting enzyme inhibition following captopril in patients with renal insuffficiency [letter]

Campbell, BC; Shepherd, AN; Elliott, HL; McLean, Kathleen; Reid, JL

doi:10.1111/j.1365-2125.1982.tb01455.x

Cited by 16 publications

(4 citation statements)

References 9 publications

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“…In contrast, our data indicate that captoprilinduced PCEA blockade is considerably lengthened by renal impairment. Thus PCEA blockade T,½2 (T½ CE) increased two-and ninefold respectively in groups 2 and 3 as compared to group 1, confirming the previous results by Campbell et al (1982a). Furthermore, there was a strong correlation between the degree of renal impairment on the one hand and T½12 CE and the overall PCEA blockade (AUCCE) on the other.…”

Section: Discussionsupporting

confidence: 86%

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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Section: Discussionsupporting

confidence: 86%

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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“…Captopril-induced inhibition of ACE activity has been demonstrated to last longer in individuals with renal failure than in healthy people. This prolongation results from persistent plasma drug levels based on the delayed renal elimination of captopril in the diseased population 23 , 24 . In infants, plasma renin activity and angiotensin II receptor expression are all much greater than in later stages of human life, and they decline during the first years of life.…”

Section: Introductionmentioning

confidence: 99%

Application of a physiologically based pharmacokinetic model in predicting captopril disposition in children with chronic kidney disease

Saifullah

Rasool

Masood

et al. 2023

Sci Rep

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Over the last several decades, angiotensin-converting enzyme inhibitors (ACEIs) have been a staple in the treatment of hypertension and renovascular disorders in children. One of the ACEIs, captopril, is projected to have all the benefits of traditional vasodilators. However, conducting clinical trials for determining the pharmacokinetics (PK) of a drug is challenging, particularly in pediatrics. As a result, modeling and simulation methods have been developed to identify the safe and effective dosages of drugs. The physiologically based pharmacokinetic (PBPK) modeling is a well-established method that permits extrapolation from adult to juvenile populations. By using SIMCYP simulator, as a modeling platform, a previously developed PBPK drug-disease model of captopril was scaled to renally impaired pediatrics population for predicting captopril PK. The visual predictive checks, predicted/observed ratios (ratiopred/obs), and the average fold error of PK parameters were used for model evaluation. The model predictions were comparable with the reported PK data of captopril in mild and severe chronic kidney disease (CKD) patients, as the mean ratiopred/obs Cmax and AUC0−t were 1.44 (95% CI 1.07 − 1.80) and 1.26 (95% CI 0.93 − 1.59), respectively. The successfully developed captopril-CKD pediatric model can be used in suggesting drug dosing in children diagnosed with different stages of CKD.

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“…This drug has been shown to be effective in lowering arterial blood pressure in many forms of hypertension [1][2][3][4], It is reported that captopril was mainly eliminated by urinary excretion [5], the elimi nation half-life of captopril from the blood was signifi cantly prolonged [6], and the duration of ACE inhibition was significantly increased [7] in patients with renal fail ure. On the other hand, captopril was eliminated by regular hemodialysis [8] and proved to be an important therapeutic entity in the treatment of refractory hyperten sion in patients on hemodialysis [9], Recently, many patients with chronic renal failure have been treated by continous ambulatory peritoneal dialysis (CAPD).…”

Section: Introductionmentioning

confidence: 99%

Pharmacokinetics and Pharmacodynamics of Captopril in Patients Undergoing Continuous Ambulatory Peritoneal Dialysis

Fujimura¹,

Kajiyama²,

Ebihara³

et al. 1986

Nephron

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Pharmacokinetics and pharmacodynamics of captopril were studied in 5 continuous ambulatory peritoneal dialysis (CAPD) patients (including 2 hypertensive patients) after single oral administration of 50 mg captopril. The pharmacokinetic parameters for plasma free unchanged captopril were time to maximal concentration 1.1 ± 0.3 h, maximal plasma concentration 387 ± 75 ng·ml^-1, elimination half-life 1.0 ± 0.3 h, and the area under the concentration-time curve 711 ± 144 ng·h•ml^-1. For plasma total captopril (the sum of free unchanged captopril and its disulfide compounds) the values were time to maximal concentration 3.5 ± 0.6 h and maximal plasma concentration 2,777 ± 429 ng·ml^-1. Captopril was detected in the dialysis fluid in all CAPD patients. Blood pressures in the 2 hypertensive CAPD patients were lower at 24 h after than before captopril administration. These results suggest that captopril may be eliminated by CAPD. In addition, there is a possibility that the antihypertensive effects of captopril may be prolonged in hypertensive CAPD patients.

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Prolonged converting enzyme inhibition following captopril in patients with renal insuffficiency [letter]

Cited by 16 publications

References 9 publications

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

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

Application of a physiologically based pharmacokinetic model in predicting captopril disposition in children with chronic kidney disease

Pharmacokinetics and Pharmacodynamics of Captopril in Patients Undergoing Continuous Ambulatory Peritoneal Dialysis

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