In vivo effect of indomethacin to potentiate the renal medullary cyclic AMP response to vasopressin.

Lum, Gary; Aisenbrey, Gary A.; Dünn, Michael J.; Berl, Tomás; Schrier, Robert W.; McDonald, Keith M.

doi:10.1172/jci108624

Cited by 118 publications

(30 citation statements)

References 20 publications

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“…Furthermore, it has been demonstrated that urinary PGE excretion increases after vasopressin administration in rabbits (23) and rats (24). In view of the foregoing observations (10,(20)(21)(22)(23)(24), we suggest that vasopressin-stimulated PGE biosynthesis inhibits vasopressin-stimulated water flow in the mammalian kidney as well as the toad urinary bladder. 1346 R. M. Zusman, H. R. Keiser, and J. S. Handler …”

Section: Resultsmentioning

confidence: 69%

See 1 more Smart Citation

Vasopressin-stimulated prostaglandin E biosynthesis in the toad urinary bladder. Effect of water flow.

Zusman¹,

Keiser²,

Handler³

1977

J. Clin. Invest.

121

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Section: Resultsmentioning

confidence: 69%

“…4) may apply to the mammalian kidney. Indomethacin enhances the in vivo antidiuretic effect of vasopressin in man (20), in the dog (21), and in the rat (22). Furthermore, it has been demonstrated that urinary PGE excretion increases after vasopressin administration in rabbits (23) and rats (24).…”

Section: Resultsmentioning

confidence: 99%

Vasopressin-stimulated prostaglandin E biosynthesis in the toad urinary bladder. Effect of water flow.

Zusman¹,

Keiser²,

Handler³

1977

J. Clin. Invest.

121

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“…Since prostaglandins are produced in the renal medulla and have been suggested to regulate blood flow in this area (15), studies were performed to evaluate the effect of administration of inhibitors of prostaglandin synthesis on the changes which occur after papillary exposure. The administration of indomethacin or meclofenamate in doses shown, to inhibit prostaglandin synthesis in the rat kidney, at least for the former compound, (16)(17)(18) prevented both the rise in PPF and the fall in Uosm (Fig. 7), suggesting the possibility that exposure of the papilla may lead to an increased PPF by a prostaglandin-mediated pathway.…”

Section: Introductionmentioning

confidence: 88%

“…There are a number of in vivo (16,19,20) and in vitro (21)(22)(23) studies which seem to demonstrate that prostaglandiin E antagonizes the hydro-osrinotic effect of vasopressini. The in vivo stuidies have beeni performed on a backgrounid of water (liuresis, a situation in which papillary tonicity is low (24).…”

Section: Introductionmentioning

confidence: 99%

Studies on the Mechanism of Reduced Urinary Osmolality after Exposure of the Renal Papilla

Chuang¹,

Reineck²,

Osgood³

et al. 1978

J. Clin. Invest.

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A B S T R A C T Studies were performiied in MlunichWistar rats to determine whether chaniges in papillary plasma flow might be responsible for the conicentrating defect which occurs after exposure of the extrarenal papilla. Papillary plasma flow was measured by 1251_ albumin accutnmulation. Initial studies in hydropenic animals revealed that papillary plasma flow was 40% higher in the kidney with the exposured papilla, 41 vs. 29 ml/min per 100 g of papilla (P < 0.001). This increase in papillary plasma flow was detectable 15 or 45 min after renmoving the ureter. Because it was unclear whether the rise in papillary plasnma flow was a cause or the result of the fall in urine osmolality, similar studies were performed in animals undergoing a water diuresis. In this setting, papillary plasma flow still increased on the exposed side compared to the control side, 81 vs. 60 ml/min per 100 g, despite similarly low uirine osmolalities of 155 and 174 mosmol/kg, respectively. This finding is compatible with the possibility that papillary exposure per se causes an increase in papillary plasma flow and that this hemodynamic alteration may lead to a reduction in urinary osmolality secondary to washout of the medullary interstitium. A final group of hydropenic rats was given either indomethacin or meclofenamate before removing the ureter. In these studies, there was no difference in either the papillary plasma flow or the urine osmolality between control and exposed kidneys. It is therefore suggested that opening the ureter induces an increase in papillary plasma flow by some mechanism which may involve an alteration in prostaglandiin synthesis.

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“…However, in the rat, doses of indomethacin which inhibit renal medullary prostaglandin synthesis do not inhibit phosphodiesterase activity (Lum et al 1977), and doses of aspirin which do not alter phosphodiesterase activity have effects identical to those of indomethacin on renal function .…”

Section: Dtscussionmentioning

confidence: 96%

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

Haylor¹,

Lote²

1980

The Journal of Physiology

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SuMMARY1. Conscious rats, with implanted carotid arterial cannulae, received a saline infusion (5.8 ml./hr) via a tail vein for a 6 hr period. The urinary excretion of water, sodium, potassium, urea and the osmolal output were monitored, together with the systemic blood pressure. Glomerular filtration rate (inulin clearance) and effective renal plasma flow (p-aminohippurate clearance) were also measured. Four hours after the start of the infusion, indomethacin (10 mg/kg body weight) in buffered saline, or buffered saline alone, was a inistered via the tail vein.2. Following indomethacin administration, urine flow, sodium output and osmolal output were markedly reduced (P < 0.01). However, there were no measurable changes in the systemic blood pressure, glomerular filtration rate, or effective renal plasma flow.3. It is concluded that the changes in urinary excretion observed after indomethacin are not dependent on changes in effective renal plasma flow or glomerular filtration, and it is suggested that indomethacin inhibits the synthesis of endogenous prostaglandins which directly influence renal tubular function.

show abstract

In vivo effect of indomethacin to potentiate the renal medullary cyclic AMP response to vasopressin.

Cited by 118 publications

References 20 publications

Vasopressin-stimulated prostaglandin E biosynthesis in the toad urinary bladder. Effect of water flow.

Vasopressin-stimulated prostaglandin E biosynthesis in the toad urinary bladder. Effect of water flow.

Studies on the Mechanism of Reduced Urinary Osmolality after Exposure of the Renal Papilla

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

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