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Research Article Free access | 10.1172/JCI117403

Bicarbonate transport along the loop of Henle. II. Effects of acid-base, dietary, and neurohumoral determinants.

G Capasso, R Unwin, F Ciani, N G De Santo, G De Tommaso, F Russo, and G Giebisch

Faculty of Medicine, 1st. University of Naples, Italy.

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Faculty of Medicine, 1st. University of Naples, Italy.

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Faculty of Medicine, 1st. University of Naples, Italy.

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Faculty of Medicine, 1st. University of Naples, Italy.

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Faculty of Medicine, 1st. University of Naples, Italy.

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Faculty of Medicine, 1st. University of Naples, Italy.

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Faculty of Medicine, 1st. University of Naples, Italy.

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Published August 1, 1994 - More info

Published in Volume 94, Issue 2 on August 1, 1994
J Clin Invest. 1994;94(2):830–838. https://doi.org/10.1172/JCI117403.
© 1994 The American Society for Clinical Investigation
Published August 1, 1994 - Version history
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Abstract

The loop of Henle contributes to renal acidification by reabsorbing about 15% of filtered bicarbonate. To study the effects on loop of Henle bicarbonate transport (JHCO3) of acid-base disturbances and of several factors known to modulate sodium transport, these in vivo microperfusion studies were carried out in rats during: (a) acute and chronic metabolic acidosis, (b) acute and chronic (hypokalemic) metabolic alkalosis, (c) a control sodium diet, (d) a high-sodium diet, (e) angiotensin II (AII) intravenous infusion, (f) simultaneously intravenous infusion of both AII and the AT1 receptor antagonist DuP 753, (g) acute ipsilateral mechanicochemical renal denervation. Acute and chronic metabolic acidosis increased JHCO3; acute metabolic alkalosis significantly reduced JHCO3, whereas chronic hypokalemic alkalosis did not alter JHCO3. Bicarbonate transport increased in animals on a high-sodium intake and following AII administration, and the latter was inhibited by the AII (AT1) receptor antagonist DuP 753; acute renal denervation lowered bicarbonate transport. These data indicate that bicarbonate reabsorption along the loop of Henle in vivo is closely linked to systemic acid-base status and to several factors known to modulate sodium transport.

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