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Corticosteroid regulation of sodium and potassium transport in the rat distal colon during postnatal development

Corticosteroid regulation of sodium and potassium transport in the rat distal colon during postnatal development

Journal of Developmental Physiology (Eynsham) 10(6): 531-540

To study the role of corticosteroids in the regulation of colonic electrogenic amiloride-sensitive Na+ absorption (IscNa) and barium-sensitive K+ secretion (IscK) during development, we investigated suckling (10-day old), weanling (25-day old) and adult (90-day old) adrenalectomized rats after they had received aldosterone, dexamethasone or corticosterone. Adrenalectomy reduced markedly IscNa in suckling rats and completely inhibited IscNa in weanling animals; the IscNa was absent in intact adults rats. The doses of aldosterone, corticosterone and dexamethasone estimated to be equivalent to the endogenus production rate of aldosterone and corticosterone restored IscNa after 1 day in both suckling and weanling rats. Compared with aldosterone, glucocorticoids produced a greater increase in IscNa. Concurrent spironolactone treatment (a mineralocorticoid antagonist) completely prevented the effect of aldosterone but had no effect in dexamethasone-treated rats. The glucocorticoid antagonist RU 38 486 inhibited the dexamethasone-induction of IscNa but had no effect on aldosterone. The response to corticosteroids, measured as the increase of IscNa, declined from suckling the adult rats. In contrast to IscNa, the same time of treatment and the same doses of corticosteroids did not influence IscK. IscK was stimulated only after chronic treatment (4 days). These findings suggest that, in the distal colon of young rats, (1) both corticosteroids may regulate amiloride-sensitive Na+ absorption and barium-sensitive K+ secretion, (2) different receptors mediate the colonic effects of glucocorticoids and mineralocorticoids, (3) immature rats are more sensitive to corticosteroids than adult animals, and (4) the acute effect of corticosteroids is an increase in Na+ absorption which is followed by delayed stimulation of K+ secretion.

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