Renal effect of prostaglandin synthetase inhibition in rats: micropuncture studies

Roman, Richard J.; Kauker, Michael L.

doi:10.1152/ajprenal.1978.235.2.f111

Cited by 29 publications

(21 citation statements)

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“…That there was no effect of either of these agents on proximal chloride reabsorption is in agreement with other micropuncture studies (11,12). The significant increase in chloride reabsorption observed between the late proximal and early distal tubule ("short loop of Henle") after indomethacin could be a result of increased reabsorption in either the superficial pars recta, the thin descending limb of Henle, or the thick ascending limb of Henle.…”

Section: Discussionsupporting

confidence: 90%

Cortical and Papillary Micropuncture Examination of Chloride Transport in Segments of the Rat Kidney during Inhibition of Prostaglandin Production

Higashihara¹,

Stokes²,

Kokko³

et al. 1979

J. Clin. Invest.

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Section: Discussionsupporting

confidence: 90%

Cortical and Papillary Micropuncture Examination of Chloride Transport in Segments of the Rat Kidney during Inhibition of Prostaglandin Production

Higashihara¹,

Stokes²,

Kokko³

et al. 1979

J. Clin. Invest.

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“…The absolute and fractional excretions of sodium, water, and chloride, GFR, and SNGFR were calculated using standard formulas. 13 The percentage of the filtered water load remaining at various points along the nephron was calculated as 100 x PJ¥ m , where P in and F^ represent the concentration of inulin in the plasma and tubular fluid samples, respectively. The percentage of the filtered chloride load remaining at the puncture site was calculated as 100 x (F a /P a )/(F in /PJ, where F a and P a represent the concentration of chloride in the tubular fluid and plasma and F in and P ta represent the concentration of inulin in the tubular fluid and plasma.…”

Section: Methodsmentioning

confidence: 99%

Pressure-diuresis in volume-expanded rats. Tubular reabsorption in superficial and deep nephrons.

Roman

1988

Hypertension

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SUMMARY Micropuncture experiments were performed in volume-expanded rats to better define the nephron segments in which changes in renal perfusion pressure inhibit tubular reabsorption. Neural influences on the kidney were eliminated by renal denervation, and plasma levels of vasopressin, aldosterone, cortkosterone, and norepinephrine were maintained at fixed levels by i.v. infusion. Fractional excretion of sodium, chloride, and water increased markedly after renal perfusion pressure was elevated from 110 to 150 mm Hg. Renal blood flow, glomerular filtration rate, and single nephron glomerular filtration rate measured from deep and superficial nephrons were unaltered. Reabsorption of chloride and water in the proximal tubule of superficial nephrons decreased by 10% after renal perfusion pressure was elevated and contributed to the pressure-diuretic response. Changes in renal perfusion pressure also altered the reabsorption of water and chloride in juxtamedullary nephrons. The percentage of the filtered water load reaching the tip of the loop of Henle increased from 19.8 ± 2.9 to 38.1 ± 3.0% after renal perfusion pressure was elevated. Chloride delivery rose from 34.

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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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Renal effect of prostaglandin synthetase inhibition in rats: micropuncture studies

Cited by 29 publications

References 0 publications

Cortical and Papillary Micropuncture Examination of Chloride Transport in Segments of the Rat Kidney during Inhibition of Prostaglandin Production

Cortical and Papillary Micropuncture Examination of Chloride Transport in Segments of the Rat Kidney during Inhibition of Prostaglandin Production

Pressure-diuresis in volume-expanded rats. Tubular reabsorption in superficial and deep nephrons.

Prostaglandin synthesis and renal function in man.

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