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

Haylor, J.; Lote, Christopher J.

doi:10.1113/jphysiol.1980.sp013087

Cited by 49 publications

(38 citation statements)

References 36 publications

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“…Several mechanisms have been suggested to account for the natriuretic and diuretic properties of prostaglandins, including an increase in total renal blood flow, and its distribution to the medulla (McGiff & Malik, 1976), antagonism of the action of antidiuretic hormone (Berl et al 1977), or a more direct action on the renal tubule (Roman & Kauker, 1978;Haylor & Lote, 1980).…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin synthesis and renal function in man.

Haylor¹

1980

The Journal of Physiology

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SUMMARY1. Experiments were performed to determine the changes in renal function which occur following prostaglandin synthetase inhibition in healthy conscious humans. It was hoped that such experiments could provide information on the mechanism by which renal prostaglandin synthesis influences urinary excretion.2. In water-diuretic male subjects (receiving a slow saline infusion) the renal excretion of sodium and water was reduced following i.v. acetylsalicylic acid (1 g) administration, while the effective renal plasma flow (p-aminohippurate clearance), and glomerular filtration rate (inulin clearance) remained unaltered. 3. In normally hydrated female subjects on an unrestricted diet, the mean urinary prostaglandin E output was 8-5 ng/hr. The renal excretion of sodium, water and urinary prostaglandin E were significantly reduced (P < 0.05) following oral acetylsalicylic acid (1 -2 g) administration.4. In normally hydrated female subjects on an unrestricted diet the renal excretion of sodium and water was reduced following oral paracetamol (1-5 g) administration.5. It is concluded that following renal prostaglandin synthetase inhibition in conscious humans, the excretion of sodium and water can be reduced without measurable changes in the glomerular filtration rate or effective renal plasma flow. It is suggested that in conscious healthy humans, the kidney may continually synthesize prostaglandin which might help to maintain sodium and water excretion by a direct action on the renal tubule without influencing renal blood flow. The relevance of this hypothesis to the intrarenal location of prostaglandin synthetase is discussed.

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Section: Introductionmentioning

confidence: 99%

Prostaglandin synthesis and renal function in man.

Haylor¹

1980

The Journal of Physiology

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“…The reason for the small changes may be due to the dose used, which might be somewhat low for this species, although our earlier study with naproxen, using a similar human dose, revealed significant increases in urine flow (17). Although studies with higher doses could help clarify this, indomethacin, nevertheless, has been shown to decrease urine output in conscious rats (13,18). This effect of indomethacin on urine flow has been attributed to its ability to inhibit prostaglandin synthesis, in particular prostaglandin E 2 (PGE 2 ), which inhibits vasopressin-stimulated water reabsorption in the collecting duct via EP3 receptor activation (19,20).…”

Section: Discussionmentioning

confidence: 99%

Comparative Effects of Indomethacin and Nabumetone on Urine and Electrolyte Output in Conscious Rats

2005

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Abstract. The effects of indomethacin and nabumetone on urine and electrolyte excretion in conscious rats were examined. Male Sprague-Dawley rats were housed individually for a fiveweek duration, consisting of acclimatization, control, experimental, and recovery phases. During the experimental phase, rats were given either indomethacin (1.5 mg ⋅ kg −1 body weight ⋅ day −1 in 0.5 ml saline, n = 10), nabumetone (15 mg ⋅ kg −1 body weight ⋅ day −1 0.5 ml saline, n = 10), or 0.5 ml saline alone (n = 10) for a period of two weeks. Water and food intake, body weight, urine output, and electrolyte excretions were estimated. Data were analyzed using two-way ANOVA. Urine output in the indomethacin-and nabumetone-treated groups was not different from the controls, but was significantly different between the drug-treated groups (P<0.01). Sodium, potassium, calcium, and magnesium excretions were not different between nabumetone-treated and control rats. However, sodium and potassium excretion was significantly lower in rats receiving indomethacin when compared to the control rats. Calcium and magnesium outputs, although did not differ from the controls, nevertheless decreased significantly with indomethacin (P<0.01). It appears that indomethacin and nabumetone when given at maximum human therapeutic doses may affect urine and electrolyte output in conscious rats.

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“…Non-myelinated axons (diameter 0-15-0-82 fum) with varicose terminals (serially sectioned) were identified as being (i) typically noradrenergic (cf. Ballard, 1978) In the conscious rat, the ability of indomethacin to increase the renal concentration gradient and reduce urine flow in the absence of changes in renal haemodynamics has been explained by prostaglandin synthetase inhibition altering renal tubular reabsorption at a distal nephron site (Haylor & Lote, 1979, 1980. In the present experiments we have investigated the action of PGE2 on renal function, and on the corticomedullary sodium gradient, in anaesthetized rats.…”

Section: P Physiological Society December 1979mentioning

confidence: 99%

Communications

1980

The Journal of Physiology

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

Cited by 49 publications

References 36 publications

Prostaglandin synthesis and renal function in man.

Prostaglandin synthesis and renal function in man.

Comparative Effects of Indomethacin and Nabumetone on Urine and Electrolyte Output in Conscious Rats

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