EFFECT OF POTASSIUM INTAKE ON THE FINAL STEPS OF ALDOSTERONE BIOSYNTHESIS IN THE RAT

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Abstract
Incubated capsular adrenal glands (»zona glomerulosa«) of potassiumdeficient rats converted 57% less tritiated deoxycorticosterone to 11β-hydroxycorticosteroids and 45 % less tritiated cortexolone to cortisol than the capsular adrenals of potassium-replete rats. A similarly decreased conversion of cortexolone to cortisol was observed when capsular adrenal mitochondria were incubated. Potassium deficiency resulted in only a slight decrease in the rate of 11β-hydroxylation by decapsulated adrenals (»zona fasciculata-reticularis«). These findings indicate that the 11β-hydroxylase activity of the zona glomerulosa of the rat adrenal cortex is dependent on the potassium intake but to a lesser extent than 18-hydroxylase activity. We had previously observed that potassium deficiency induced a decreased production of aldosterone, an unchanged corticosterone output and an increased deoxycorticosterone output by capsular adrenals incubated with stimulating agents. The same alterations in endogenous corticosteroid production could be induced in vitro by the addition of a selective inhibitor of 18-hydroxylation (Su 8000) to the incubation medium. On the other hand, metopirone, i.e. an inhibitor of both 11β- and 18-hydroxylation, diminished corticosterone as well as aldosterone output by capsular adrenals. These results suggest that an increased deoxycorticosterone output by capsular adrenals may be due not only to a decrease in 11β-hydroxylase activity but may also be indirectly related to a decreased conversion of corticosterone to 18-hydroxycorticosterone and aldosterone.

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