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Since the isolation of angiotensin from dog plasma 30 years ago, investigators have devoted considerable effort to elucidating the mechanism of regulation of renin secretion. Initially, attention was directed at the role of renal arterial pressure, or pulse pressure as the regulating factor. However, more recent studies, using a refined technique for measuring renin activity, demonstrate that renin secretion can vary quite independently of arterial (1) or pulse pressure changes (2). A number of reports appear to stress the role of the autonomic nervous system (1, 3-5), body sodium or volume changes (6, 7), and intrarenal mechanisms unrelated to blood pressure changes. Because of their anatomical and functional relation to the renin secreting cells of the juxtaglomerular apparatus, the macula densa cells of the distal tubule have been considered to be involved in the intrarenal regulation of renin secretion (8-11). The sodium concentration of the tubular fluid or sodium reabsorption at this site may in some way affect renin release. Part I of the present study was designed to examine the role of this intrarenal mechanism, namely, to see the effect of changing distal sodium reabsorption on renin secretion. It was found that the saluresis brought on by administration of chlorothiazide in the dog resulted within 15 min in an increased secretion of renin even when urinary loss of water and salt was replaced. Part II therefore was undertaken to see whether this same effect of chlorothiazide obtained in man and whether this effect was under the influence of the autonomic nervous system. The effect of the diuretic on peripheral renin activity was measured before and after neuronal depletion of catecholamines induced by chronic reserpine administration.
Slotkoff et al. (1971) studied this question.