The Effect of Indomethacin on Kidney Function and Plasma Renin Activity in Man

Donker, A. J. M.; Arisz, L.; Brentjens, Jrh; Vanderhem, Gk; Hollemans, H. J. G.

doi:10.1159/000180733

Cited by 270 publications

(87 citation statements)

References 12 publications

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“…In fact, the initial NO synthesis inhibition at a perfusion pressure of 125 ± 5 mmHg was followed by a significant decrease in TRBF as well as RMBF. In contrast to the effects observed after the blockade of NO synthesis, the inhibition of PG synthesis is followed by a marked reduction of renal blood flow when perfused at low, but not at high RPP levels (5,7,16,19). This is in agreement with our results showing that PG inhibition did not alter TRBF.…”

Section: Discussionsupporting

confidence: 91%

“…There is, at present, a well accepted notion that PGs (9,10) and NO (5,16,17) play an important role in the regulation of TRBF. In fact, previous studies have shown that the blockade of either NO or PG is followed by a decrease in TRBF and impairment in urine sodium excretion both under basal conditions (5,6) and during pressureinduced natriuresis (6,7,18).…”

Section: Discussionmentioning

confidence: 99%

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Role of nitric oxide and prostaglandin in the maintenance of cortical and renal medullary blood flow

Gomez

Strick

Romero

2008

Braz J Med Biol Res

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This study was undertaken in anesthetized dogs to evaluate the relative participation of prostaglandins (PGs) and nitric oxide (NO) in the maintenance of total renal blood flow (TRBF), and renal medullary blood flow (RMBF). It was hypothesized that the inhibition of NO should impair cortical and medullary circulation because of the synthesis of this compound in the endothelial cells of these two territories. In contrast, under normal conditions of perfusion pressure PG synthesis is confined to the renal medulla. Hence PG inhibition should predominantly impair the medullary circulation. The initial administration of 25 µM kg -1 min -1 NG-nitro-L-arginine methyl ester produced a significant 26% decrease in TRBF and a concomitant 34% fall in RMBF, while the subsequent inhibition of PGs with 5 mg/kg meclofenamate further reduced TRBF by 33% and RMBF by 89%. In contrast, the initial administration of meclofenamate failed to change TRBF, while decreasing RMBF by 49%. The subsequent blockade of NO decreased TRBF by 35% without further altering RMBF. These results indicate that initial PG synthesis inhibition predominantly alters the medullary circulation, whereas NO inhibition decreases both cortical and medullary flow. This latter change induced by NO renders cortical and RMBF susceptible to a further decrease by PG inhibition. However, the decrease in medullary circulation produced by NO inhibition is not further enhanced by subsequent PG inhibition.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Role of nitric oxide and prostaglandin in the maintenance of cortical and renal medullary blood flow

Gomez

Strick

Romero

2008

Braz J Med Biol Res

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“…In salt deplete humans, indomethacin has been reported to have little effect on basal renal haemodynamics (Donker et al, 1976;Mackay et al, 1984;Sedor et al, 1984), but there are reports of a significant decrease (Kramer et al, 1985). There is little information available on the renal haemodynamic effect of ibuprofen.…”

Section: Introductionmentioning

confidence: 99%

The effects of ibuprofen and indomethacin on renal function in the presence and absence of frusemide in healthy volunteers on a restricted sodium diet.

Passmore¹,

Copeland²,

Johnston³

1990

Brit J Clinical Pharma

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1 Since salt depletion stimulates the renal prostaglandin system to maintain renal function, the effects of indomethacin and ibuprofen upon renal haemodynamics, electrolyte excretion and renin release were examined in eight healthy male volunteers on a salt restricted diet, before and after frusemide administration. 2 Neither indomethacin (50 mg) nor ibuprofen (400 mg and 800 mg) affected renal blood flow, glomerular filtration rate or electrolyte excretion before frusemide. 3 Renal blood flow and glomerular filtration rate were significantly increased in the first 20 min after frusemide. These changes were significantly attenuated by indomethacin compared with placebo and ibuprofen 400 mg. Frusemide-induced diuresis but not natriuresis was inhibited by all treatments. 4 Both nonsteroidal agents inhibited equally the rise in renin activity seen after frusemide. 5 In this group of healthy volunteers on a salt restricted diet, ibuprofen and indomethacin had no detrimental effects on renal function in the absence of frusemide. The changes in renal haemodynamics due to frusemide were suppressed more by indomethacin than by ibuprofen, probably reflecting the more potent nature of indomethacin as an inhibitor of prostaglandin synthesis.

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“…<4 Nevertheless, the effects of longterm treatment on renal hemodynamics resemble those found in studies of short-term treatment in that antiinflammatory drugs seem to have more effect on glomerular filtration rate than on renal blood flow. 39 -44 - VOL 8, No 8, AUGUST 1986 The different effects exerted by anti-inflammatory drugs on renal hemodynamics after short-term and long-term treatment may be partly explained by the studies of Vallatton et al, 21 who reported significant qualitative differences in the effect of indomethacin on renal function, depending on whether anti-inflammatory drugs were administered simultaneously or after the production of a negative sodium balance.…”

Section: -L0mentioning

confidence: 99%

Effects of long-term treatment with indomethacin on renal function.

Ruilope¹,

Robles²,

Payá³

et al. 1986

Hypertension

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SUMMARY The prolonged effects (42 days) of indomethacin treatment on the renin-angiotensinaldosterone axis, renal hemodynamics, and renal excretory function in humans were studied. Indomethacin produced a 41% sustained depression in the 24-hour excretion of prostaglandin E 2 and a mild (7%) decrease in inulin clearance but did not affect the clearance of p-aminohippurate, the 24-hour excretion of sodium and potassium, or the basal values of plasma aldosterone; however, it decreased the basal values of renin and prevented the stimulated (3 hours of walking) responses of plasma renin activity and plasma aldosterone. Indomethacin also produced a decrease in both the diuretic and saluretic response to furosemide and in the renal ability to concentrate urine. The indomethacin-induced hyporeninism and hypoaldosteronism were more pronounced when the subjects were receiving a sodium-restricted diet. This finding indicates that prolonged administration of anti-inflammatory drugs induces chronic hyporeninism and hypoaldosteronism. Prolonged treatment with indomethacin also produced some of the symptoms of a syndrome of hypoprostaglandinism, such as decreased plasma renin activity, plasma aldosterone, and urinary prostaglandin E 2 in association with increases in plasma potassium levels and diastolic pressure. (Hypertension 8: 677-684, 1986) KEY WORDS * renin • aldosterone • prostaglandin E 2 • furosemide • degenerative joint disease * low sodium diet R ENAL prostaglandins play an important role in mediating the release of renin 1 2 and in regu-. lating renal function, as estimated through changes in renal blood flow, M glomerular filtration rate, 7 and renal handling of sodium and water. 8 Evidence also indicates that prostaglandins have a renal protective effect, especially in situations characterized by a decrease of renal perfusion.9 " 1 ' Under normal conditions, however, blockade of prostaglandin synthesis in association with the short-term administration of nonsteroidal anti-inflammatory drugs decreases renin release without inducing a marked impairment in renal From the Department of Nephrology (L.M. Ruilope, J.M. Alcazar, E. Miravalles, and J. Rodicio), Hospital "1° de Octubre," and the Department of Endocrinology

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The Effect of Indomethacin on Kidney Function and Plasma Renin Activity in Man

Cited by 270 publications

References 12 publications

Role of nitric oxide and prostaglandin in the maintenance of cortical and renal medullary blood flow

Role of nitric oxide and prostaglandin in the maintenance of cortical and renal medullary blood flow

The effects of ibuprofen and indomethacin on renal function in the presence and absence of frusemide in healthy volunteers on a restricted sodium diet.

Effects of long-term treatment with indomethacin on renal function.

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