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1 School of Biological Sciences, University of Manchester, Manchester, United Kingdom
* To whom correspondence should be addressed. E-mail: nick.ashton{at}man.ac.uk.
Rapid, non-genomic actions of aldosterone have been demonstrated in a number of cell types in vitro, including renal cell lines, but there remains little direct evidence that it is able to exert rapid effects on the kidney in the whole animal. Accordingly, the aim of this study was to determine whether aldosterone induces rapid changes in the renal handling of electrolytes or acid-base balance in the anaesthetised rat. Using a servo-controlled fluid replacement system, spontaneous urine output by anaesthetised male Sprague Dawley rats was replaced with 2.5% dextrose. Following 3 h equilibration and 1 h control, rats were infused with aldosterone (42 pmol min-1) or vehicle for an hour. Aldosterone infusion induced a rapid (within 15 min) increase in sodium excretion which peaked at 0.24 ± 0.08 compared with 0.04 ± 0.01 mmol min-1 100 body weight-1 (P = 0.041) in the vehicle infused rats. This natriuresis was not associated with changes in glomerular filtration rate, urine flow rate, potassium, chloride or bicarbonate excretion nor urine pH. The mechanisms involved are unclear, but as we have previously shown that aldosterone stimulates a rapid (4 min) increase in cAMP generation in the rat inner medullary collecting duct (IMCD), they could involve cAMP-mediated activation of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel which drives Na+ secretion in the IMCD.
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