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Am J Physiol Renal Physiol 280: F172-F179, 2001;
0363-6127/01 $5.00
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Vol. 280, Issue 1, F172-F179, January 2001

Distal tubular electrolyte transport during inhibition of renal 11beta -hydroxysteroid dehydrogenase

Katharine J. Biller1,dagger, Robert J. Unwin2, and David G. Shirley2

1 Division of Biomedical Sciences, Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF; and 2 Centre for Nephrology, Royal Free and University College Medical School, London W1N 8AA, United Kingdom

To test the proposal that the enzyme 11beta -hydroxysteroid dehydrogenase (11beta -HSD) confers aldosterone specificity on mineralocorticoid receptors in the distal nephron by inactivating glucocorticoids, we performed a free-flow micropuncture study of distal tubular function in adrenalectomized rats infused with high-dose corticosterone. One-half of the rats were additionally given intravenous carbenoxolone (CBX; 6 mg/h) to inhibit renal 11beta -HSD activity. Although this maneuver lowered fractional Na+ excretion (1.1 ± 0.2 vs. 1.9 ± 0.2%, P < 0.01), Na+ reabsorption within the accessible distal tubule was found to be similar in the two groups of animals. In contrast, distal tubular K+ secretion was enhanced in CBX-treated rats: fractional K+ deliveries to the early and late distal collection sites in the corticosterone-alone group were 13 ± 1 and 20 ± 3%, respectively (not significant), whereas corresponding data in the CBX-treated group were 9 ± 1 and 24 ± 2% (P < 0.01). This stimulation of distal K+ secretion provides the first direct in vivo evidence that 11beta -HSD normally prevents corticosterone from exerting a mineralocorticoid-like effect in the distal tubule. The reduction in fractional Na+ excretion during inhibition of 11beta -HSD, in the absence of a change in end-distal Na+ delivery, suggests enhanced Na+ reabsorption in the collecting ducts.

carbenoxolone; sodium reabsorption; potassium secretion; micropuncture; corticosterone

dagger Deceased.




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