The influence of prostaglandin inhibition by indomethacin on blood pressure and renal function in hypertensive patients treated with cilazapril.

Kirch, Wilhelm; Stroemer, K.; Hoogkamer, J. F. W.; Kleinbloesem, C. H.

doi:10.1111/j.1365-2125.1989.tb03495.x

Cited by 21 publications

(8 citation statements)

References 15 publications

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“…However, the degree of attenuation was dependent on the sequence of drug administration, since it was more pronounced in patients who initially received indomethacin and then a combination of both drugs than in patients receiving the drugs in the opposite order. The investigators postulated that the effects of indomethacin may result from a reduction in plasma renin activity, prostaglandin synthesis or sodium excretion (Kirch et al 1989). Similar results of pharmacodynamic interactions with captopril or enalapril and indomethacin have been reported as occurring in healthy volunteers (Koopmans et ill. 1989).…”

Section: Nonsteroidal Anti-inflammatory Drugs (Nsaids)mentioning

confidence: 66%

“…The investigators noted that this interaction may have clinical relevance in patients not only with nephrotic kidney but also with heart failure or hypertension. Kirch et al (1989) investigated the influence of indomethacin 100mg on the antihypertensive efficacy of cilazapril 2.5mg in a placebo-controlled crossover study including 20 patients with essential hypertension in which each drug was administered for 2 weeks alone before the combination. During combined therapy, a significant attenuation of the blood pressure-lowering activity of cilazapril occurred.…”

Section: Nonsteroidal Anti-inflammatory Drugs (Nsaids)mentioning

confidence: 99%

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Pharmacokinetic Drug Interactions with ACE Inhibitors

Shionoiri

1993

Clinical Pharmacokinetics

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Angiotensin converting enzyme (ACE) inhibitors which have active moieties excreted mainly in urine require adjustment of either the dose or the interval between doses in patients with moderate to severe renal dysfunction or severe congestive heart failure. Those agents such as temocapril (CS 622) and fosinopril, excreted both in urine and bile, may not require such adjustment. Renal clearance of ACE inhibitors may be reduced and some accumulation may occur in elderly patients with mild renal dysfunction or congestive heart failure. The bioavailability of ACE inhibitors is reduced by concomitant food or antacids which may slow gastric emptying and raise gastric pH. Pharmacokinetic interactions with ACE inhibitors are unlikely in patients receiving thiazide or loop diuretics. When ACE inhibitors are given hyperkalaemia may occur in patients with renal insufficiency, those taking potassium supplements or potassium-sparing diuretics, and in diabetic patients with mild renal impairment. While no pharmacokinetic interaction precludes use of this combination, the pharmacokinetics of some ACE inhibitors are subject to greater variability when patients also receive beta-blockers. Calcium antagonists and ACE inhibitors have additive anti-hypertensive effects and pharmacokinetic interactions between these agents are unlikely. One report exists of a significant effect of coadministered hydralazine on the pharmacokinetics and urinary excretion of lisinopril. Data on interactions between ACE inhibitors and digitalis are contradictory. There is no evidence that the concomitant use of ACE inhibitors and digoxin is associated with an increased risk of digitalis toxicity. ACE inhibitors are mainly excreted by glomerular filtration and renal tubular secretion. Possible interactions between ACE inhibitors and probenecid have been noted, with renal and total body clearance of ACE inhibitors being potentially reduced in the presence of probenecid. Probenecid pretreatment may enhance the pharmacodynamic response of ACE inhibitors. Few but contradictory data exist on the effects of H2-blockers on ACE inhibitor pharmacokinetics and little information is available on interactions between ACE inhibitors and hypoglycaemic drugs. Some case reports link ACE inhibitors with the induction of lithium toxicity. Coadministration of lithium should be undertaken with caution, and frequent monitoring of lithium concentrations is recommended with all ACE inhibitors. Nonsteroidal anti-inflammatory drugs (NSAIDs) may attenuate the haemodynamic actions of ACE inhibitors. NSAIDs reduce renal excretion of ACE inhibitors, with a corresponding increase in circulating drug concentrations. There is little information available on the pharmacokinetic interaction with ACE inhibitors and cyclosporin, but caution should be employed when they are used together.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Nonsteroidal Anti-inflammatory Drugs (Nsaids)mentioning

confidence: 66%

Section: Nonsteroidal Anti-inflammatory Drugs (Nsaids)mentioning

confidence: 99%

Pharmacokinetic Drug Interactions with ACE Inhibitors

Shionoiri

1993

Clinical Pharmacokinetics

View full text Add to dashboard Cite

show abstract

“…In addition to prostaglandin inhibition, alterations of the renin-aldosterone-angiotensin system caused by the NSAIDs are involved in this interaction [3,4]. Oxaprozin only slightly decreases parameters of renal function, probably due to inhibition of cyclooxygenase activity [6,7].…”

Section: Adverse Experiencesmentioning

confidence: 97%

“…Nonsteroidal antiinflammatory drugs (NSAIDs) like indomethacin are prostaglandin inhibitors, are known to attenuate the antihypertensive effect of diuretics, beta blockers or ACE inhibitors [1][2][3][4]. In addition to prostaglandin inhibition, alterations of the renin-aldosterone-angiotensin system caused by the NSAIDs are involved in this interaction [3,4].…”

Section: Adverse Experiencesmentioning

confidence: 99%