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Research Article Free access | 10.1172/JCI106380

The effect of altered sodium concentration in the distal nephron segments on renin release

C. Robert Cooke, Torrey C. Brown, Barry J. Zacherle, and W. Gordon Walker

1Department of Medicine of The Johns Hopkins University School of Medicine and The Johns Hopkins Hospital, Baltimore, Maryland 21205

Find articles by Cooke, C. in: PubMed | Google Scholar

1Department of Medicine of The Johns Hopkins University School of Medicine and The Johns Hopkins Hospital, Baltimore, Maryland 21205

Find articles by Brown, T. in: PubMed | Google Scholar

1Department of Medicine of The Johns Hopkins University School of Medicine and The Johns Hopkins Hospital, Baltimore, Maryland 21205

Find articles by Zacherle, B. in: PubMed | Google Scholar

1Department of Medicine of The Johns Hopkins University School of Medicine and The Johns Hopkins Hospital, Baltimore, Maryland 21205

Find articles by Walker, W. in: PubMed | Google Scholar

Published September 1, 1970 - More info

Published in Volume 49, Issue 9 on September 1, 1970
J Clin Invest. 1970;49(9):1630–1638. https://doi.org/10.1172/JCI106380.
© 1970 The American Society for Clinical Investigation
Published September 1, 1970 - Version history
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Abstract

Ethacrynic acid, a potent inhibitor of sodium reabsorption in the ascending limb of Henle's loop, produces a sharp rise in renal venous renin activity within 5 min after intravenous administration in anesthetized dogs. This response persists when volume depletion is prevented by returning urinary outflow to the femoral vein. Comparable studies with chlorothiazide, a diuretic with little or no effect on the medullary portion of the ascending limb of the loop of Henle, failed to produce a significant increase in renal venous renin activity.

When administered during ureteral occlusion, ethacrynic acid produced no change in renal venous renin activity until ureteral occlusion was released and flow restored. Following release of the ureters, a prompt rise in renal venous renin was again observed within 5 min of release. Control studies of ureteral occlusion yielded a fall in renal venous renin activity following release of the ureter without administration of ethacrynic acid. These studies identify a prompt stimulatory effect of ethacrynic acid on renin release that is unrelated to volume depletion but dependent upon the presence of tubular urine flow. Although further definition of the site and characteristics of the distal tubular mechanism for stimulation of renin release requires more direct study, the data presented here indicate that changes in sodium concentration in distal tubular fluid serve as a stimulus for renin release.

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