Pharmacokinetics of angiotensin converting enzyme inhibitors.

Burnier, Michel; Waeber, Bernard; Nussberger, Jürg; Brunner, Heinrich

doi:10.1111/j.1365-2125.1989.tb03588.x

Cited by 10 publications

(3 citation statements)

References 34 publications

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“…With several ACE inhibitors, a dissociation between plasma angiotensin II levels and the antihypertensive effect has been observed during prolonged administration (Nussberger et al 1985. Possible reasons relate to other angiotensin II-dependent actions of ACE inhibitors such as an attenuation of sympathetic activity, increased parasympathetic activity and depressor hormones, and inhibition of tissue angiotensin systems operating independently of the circulating components (Burnier et al 1989;Veltmar et al 1991). Interposed humoral and vascular factors such as the renin response to ACE inhibition should also be considered; the dose-response to the ACE inhibitor trandolapril as evaluated by its effect on circulating angiotensin II levels is limited by this renin response (Mooser et al 1990).…”

Section: Essential Hypertensionmentioning

confidence: 95%

Pharmacokinetic Optimisation of Angiotensin Converting Enzyme (ACE) Inhibitor Therapy

Burnier¹,

Biollaz²

1992

Clinical Pharmacokinetics

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Angiotensin converting enzyme (ACE) inhibitors are increasingly used to treat hypertension and congestive heart failure. Recently, several new ACE inhibitors with pharmacokinetic features different from earlier agents such as captopril or enalapril have come into use. This review discusses the use of pharmacokinetics to optimise ACE inhibitory therapy in various patient groups. Among the pharmacokinetic characteristics of ACE inhibitors the route of excretion and to a lesser degree the half-life appear to be the most clinically relevant. There is no evidence that being a prodrug offers a significant clinical advantage. The importance of varying tissue penetration also remains to be determined. Knowledge of ACE inhibitor pharmacokinetics is particularly important in patients with renal or hepatic dysfunction in whom the major route of excretion of these agents is impaired. This might also be the case in elderly patients or those with severe congestive heart failure. However, for most ACE inhibitors, major changes in the drug dosage (amount or interval) are necessary only when the glomerular filtration rate falls below 30 ml/min (1.80 L/h). The occurrence of adverse effects due to overdosage or drug interactions may be prevented by adapting the prescription of an ACE inhibitor to its pharmacokinetic characteristics.

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Section: Essential Hypertensionmentioning

confidence: 95%

Pharmacokinetic Optimisation of Angiotensin Converting Enzyme (ACE) Inhibitor Therapy

Burnier¹,

Biollaz²

1992

Clinical Pharmacokinetics

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“…high pressure liquid chromatography) and subsequent sensitive All octapeptide radioimmunoassay. There is disagreement whether or not the effects of different ACE inhibitors can be compared even using the same substrate assay to detect ACE activity (Burnier et al, 1989).…”

Section: Ace Inhibitors and Tissue And Plasma Ace Analytical Aspectsmentioning

confidence: 99%

“…Interest in the renal effects of ACE inhibitor therapy is predominantly focused on the haemodynamic effects on renal function and on the possibility of detrimental effects on kidneys affected by renal artery stenosis (Burnier et al, 1989). The beneficial effects of ACE inhibitor therapy in kidneys affected by diabetic hyperfiltration (Marre et al, 1987;Romanelli et al, 1989;Taguma et al, 1985) or hypertensive nephropathy (Ikeda et al, 1989) are attributed to haemodynamic alterations (Raij et al, 1989).…”

Section: Renal and Ras And Ace Activitymentioning

confidence: 99%

Tissue and plasma angiotensin converting enzyme and the response to ACE inhibitor drugs.

Lees

Reid

1991

Brit J Clinical Pharma

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1. There is a body of circumstantial and direct evidence supporting the existence and functional importance of a tissue based RAS at a variety of sites. 2. The relation between circulatory and tissue based systems is complex. The relative importance of the two in determining haemodynamic effects is unknown. 3. Despite the wide range of ACE inhibitors already available, it remains unclear whether there are genuine differences related to tissue specificity. 4. Pathological states such as chronic cardiac failure need to be explored with regard to the contribution of tissue based ACE activities in generating acute and chronic haemodynamic responses to ACE inhibitors. 5. The role of tissue vs plasma ACE activity may be clarified by study of the relation between drug concentration and haemodynamic effect, provided that the temporal dissociation is examined and linked to circulating and tissue based changes in ACE activity, angiotensin peptides and sympathetic hormones.

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Study on pharmacokinetics of a new biliary excreted oral angiotensin converting enzyme inhibitor, temocapril (CS‐622) in humans

Suzuki

Kawaratani

Shioya

et al. 1993

Biopharm & Drug Disp

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Despite the usefulness of angiotensin converting enzyme (ACE; EC 3.4.15.1) inhibitors for patients with renal insufficiency, some hesitation has been exercised in applying ACE inhibitors to the treatment of such patients because most ACE inhibitors are excreted mainly into the urine. In this context, development of an ACE inhibitor which is excreted into the bile has been sought. The pharmacokinetic properties of the novel ACE inhibitor, temocapril hydrochloride (temocapril HCl; CS-622), were investigated in six healthy volunteers. This drug is excreted mainly into the bile in animal studies. Temocapril HCl was given in a single dose of 0.5, 1.0, and 2.0 mg, and 36, 44, and 38 per cent of the administered drug was excreted in the feces and 17, 19, and 24 per cent in the urine as the de-esterified active diacid form (the diacid metabolite) within 48 h, respectively. The plasma ACE activity was markedly inhibited. No abnormal clinical findings suggestive of side-effects were observed. Thus, from the pharmacokinetic standpoint, temocapril HCl is expected to be a useful drug for patients with renal dysfunction.

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Pharmacokinetics of angiotensin converting enzyme inhibitors.

Cited by 10 publications

References 34 publications

Pharmacokinetic Optimisation of Angiotensin Converting Enzyme (ACE) Inhibitor Therapy

Pharmacokinetic Optimisation of Angiotensin Converting Enzyme (ACE) Inhibitor Therapy

Tissue and plasma angiotensin converting enzyme and the response to ACE inhibitor drugs.

Study on pharmacokinetics of a new biliary excreted oral angiotensin converting enzyme inhibitor, temocapril (CS‐622) in humans

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