Sulindac. A potentially renal-sparing nonsteroidal anti-inflammatory drug

Bunning, Robert D.; Barth, Werner F.

doi:10.1001/jama.248.21.2864

Cited by 57 publications

(25 citation statements)

References 17 publications

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“…Sulindac was studied because of the suggested lack of inhibition of renal pros taglandins in comparison to other NSAIDs such as indomethacin and ibuprofen [16][17][18][19]. Our results suggest that, in healthy males on a normal sodium diet, the natriuretic response to intravenous furosemide was not inhibited by either ibuprofen or sulindac, while both agents significantly suppressed the stimulation of plasma renin activity.…”

mentioning

confidence: 70%

Sulindac and Ibuprofen Inhibit Furosemide-Stimulated Renin Release but not Natriuresis in Men on a Normal Sodium Diet

Riley¹,

Vlasses²,

Rotmensch³

et al. 1985

Nephron

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We compared the effect of two commonly prescribed nonsteroidal anti-inflammatory drugs, ibuprofen and sulindac, and placebo on intravenous furosemide-induced natriuresis and renin stimulation in 11 healthy male volunteers, consuming a 100 mEq sodium, 80 mEq potassium diet. Chronic (6-day) therapy with each agent was followed by a 1-week washout period. There were no significant treatment-related differences in either urine volume or sodium excretion for any of the designated collection periods or for the cumulative value for the 4 h after furosemide administration. Similarly, differences among groups were not observed for creatinine clearance, urinary potassium and urinary chloride excretion. Mean basal plasma renin activity levels prior to furosemide administration on day 6 were significantly lower in the presence of ibuprofen (1.5 ± 2.0 ng/ml/h; p < 0.01) and sulindag (2,3 ± 0.9 ng/ml/h; p < 0.05), compared with placebo (3.3 ± 1.1 ng/ml/h); the difference between the two NSAIDs was also significant (p < 0.05). Mean plasma renin activity levels in the 4 h after furosemide increased significantly at all time points in comparison to basal values, but were significantly less for ibuprofen and sulindac groups in the first hour. Our data suggest that the natriuresis following intravenous furosemide in men consuming a normal sodium intake is not prostaglandin-dependent. Furthermore, the observation that sulindac suppressed basal and stimulated plasma renin activity levels, albeit to a lesser extent than ibuprofen, questions the claim that sulindac ‘spares’ the kidney and compels further evaluation of this issue.

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mentioning

confidence: 70%

Sulindac and Ibuprofen Inhibit Furosemide-Stimulated Renin Release but not Natriuresis in Men on a Normal Sodium Diet

Riley¹,

Vlasses²,

Rotmensch³

et al. 1985

Nephron

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“…Ciabattoni et al (1980) have first reported that sulindac may be unique because it does not inhibit renal PG synthesis in normal volunteers and in a patient with Bartter's syndrome as measured by urinary PG excretion. These observations were later confirmed by several studies in normal subjects and in patients with chronic glomerular disease or hypertension (Bunning and Barth 1982;Salvetti et al 1982; Ciabattoni et al 1984; Sedor et al 1984; Puddey et al 1985; Vriesendorp et al 1986a). Recently, however, there are controversial results indicating that sulindac reduces urinary excretion of PGE2 and is not specifically renalsparing both in experimental animals and in healthy subjects or in patients with renal, liver of cardiac diseases (Berg and Talseth 1985;Brater et al 1985; Olanoff et al 1985; Roberts et al 1985;Laf et al 1986).…”

mentioning

confidence: 70%

Effect of Sulindac on Prostaglandin Synthesis in Human and in Cultured Rat Renal and Vascular Smooth Muscle Cells.

Sato¹,

Abe

Takeuchi³

et al. 1992

Tohoku J. Exp. Med.

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To examine the hypothesis that Sulindac does not inhibit renal prostaglandin (PG) synthesis, we investigated the effects of Sulindac and other nonsteroidal anti-inflammatory drugs on PG synthesis in human and in cultured rat renal and vascular smooth muscle (VSM) cells. In 7 patients with chronic glomerular disease, creatinine clearance and proteinuria were not changed by Sulindac but were significantly reduced by diclofenac sodium. However, urinary excretion of PGE2 was decreased by both drugs. In cultured glomerular mesangial (GM), renal papillary collecting tubule (RPCT) and VSM cells from mesenteric artery, indomethacin, tiaprofenic acid, aspirin and ibuprofen inhibited both basal and arachidonic acid (AA)-stimulated PG synthesis dose-dependently. Although Sulindac sulfoxide, at the same concentrations, inhibited both basal and AAstimulated PGE2 synthesis in RPCT cells, it was less potent to inhibit PGI2 synthesis in VSM cells or PGE2 synthesis in GM cells. Active form sulindac sulfide inhibited PG synthesis in all types of cells but its inactive form sulfone did not. We conclude that sulindac inhibits renal PG synthesis but has little effect on renal function. This may be explained by its relatively weak potency on glomerular or vascular PG synthesis inhibition possibly due to the different biotransformation of the sulfoxide to the active sulfide in these cells.sulindac ; prostaglandin synthesis ; renal-sparing effect ; renal cells ; nonsteroidal antiinflammatory drug Nonsteroidal anti-inflammatory drugs (NSAIDs) are the agents which are most frequently used in a variety of disease. As the number of patients taking NSAIDs increases, there are numerous reports on renal and electrolyte disturbances and attenuation of the hypotensive effect of antihypertensive drugs such as

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“…The result indicates that sulindac as well as diclofenac sodium does not interfere with BP control obtained by nifedipine, despite of reduced renal PGEZ synthesis. On the other hand, sulindac has been shown to be a renal sparing drug (Bunning and Barth 1982 ;Sedor et al 1984 ;Ciabattoni et al 1984). The rare adverse effect of sulindac on renal function is due to less inhibition of renal PG synthesis, although the inhibitory effect of sulindac on renal PG synthesis is still controversial (Patrono and Dunn 1987; Stillman and Schlesinger 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Hence, more careful evaluation about the effect of NSAIDs on BP control is required. On the other hand, sulindac is shown to have a rare side effect on renal function (Bunning and Barth 1982;Ciabattoni et al 1984;Sedor et al 1984). It may also be probable that sulindac has no adverse affect on hypertension treatment that favors renal function.…”

mentioning

confidence: 99%

No Adverse Effect of Non-Steroidal Anti-Inflammatory Drugs, Sulindac and Diclofenac Sodium, on Blood Pressure Control with a Calcium Antagonist, Nifedipine, in Elderly Hypertensive Patients.

Takeuchi¹,

Abe

Yasujima³

et al. 1991

Tohoku J. Exp. Med.

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Sulindac. A potentially renal-sparing nonsteroidal anti-inflammatory drug

Cited by 57 publications

References 17 publications

Sulindac and Ibuprofen Inhibit Furosemide-Stimulated Renin Release but not Natriuresis in Men on a Normal Sodium Diet

Sulindac and Ibuprofen Inhibit Furosemide-Stimulated Renin Release but not Natriuresis in Men on a Normal Sodium Diet

Effect of Sulindac on Prostaglandin Synthesis in Human and in Cultured Rat Renal and Vascular Smooth Muscle Cells.

No Adverse Effect of Non-Steroidal Anti-Inflammatory Drugs, Sulindac and Diclofenac Sodium, on Blood Pressure Control with a Calcium Antagonist, Nifedipine, in Elderly Hypertensive Patients.

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