Abstract
Summary
In unilaterally nephrectomized rabbits, cortexone and salt administration reduces renin content and the juxtaglomerular granulation index of the kidney and does not provoke hypertension. Renal artery clamping induces a rise in blood pressure without causing changes in renin content nor JGI, which remain normal. Combination of these 2 experimental procedures is followed by hypertension and a decrease in renin content and JGI. The width of the adrenal zona glomerulosa is reduced under the influence of cortexone and salt, and remains unaffected by renal artery constriction. In the rabbit, therefore, mineralocorticoids seem to play no major role in induction of renal hypertension. Neither does renin appear as a necessary agent in the mechanism responsible for the development of renal hypertension.
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