Abstract
Juxtaglomerular index, renal pressor activity and width of the zona glomerulosa were normal in unilaterally nephrectomized hypertensive rats maintained on a normal sodium intake, increased in those subjected to sodium depletion and decreased in those receiving 1% saline. This indicates that renin formation and secretion are most likely the result of the sodium state of the animal rather than loss of a renin-stimulating agent in the contralateral or unclipped kidney. Failure of sodium to influence the degree of hypertension in unilaterally nephrectomized hypertensive rats militates against a direct quantitative relationship between blood pressure and the renin-angiotensin-aldosterone system.
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