Renin and the sympathetic nervous system.

Abstract

Fig. 1, from a review by Davis [1], is shown as a useful frame of reference to indicate the two basic mechanisms which have alternatively been suggested as responsible for stimulating the juxtaglomerular apparatus to secrete or release renin. The so-called stretch-receptor or baroceptor hypothesis, first advanced by Tobian [2] and by Skinner, McCubbin and Page [3], maintains that the juxtaglo-merular cells not only represent the producing site of renin, but also a sensor responsive to stretch of the afferent arteriole, in such a way that a stretch of the arteriole wall inhibits refill release. An alternative hypothesis, the so-called natrioceptive hypothesis, was first advanced by Vander [4, 5] and maintains that the primary receptors lie in the macula densa. These specific cells of the distal tubule would be responsive to the sodium in the tubular fluid, either to the sodium load (and presumably to intracellular sodium transport) according to Vander [6] or to sodium concentration in the tubular fluid according to Thurau [6, 8]. The relative role of the renal vascular receptor and of the macula densa has been recently assessed by Davis and his group [9] in the non-filtering kidney preparation: their present position is that there is a double intrarenal receptor system, to which both baro- and natrioceptive mechanisms contribute, but that in most instances the baroceptor is by far the most important mechanism [9]. Open image in new window Fig. 1. Diagram of the juxtaglomerular apparatus, with indication of the vascular stretch receptor in the afferent arteriole, and of the natrioceptors in the macula densa. (From Davis, 1, by courtesy of the American Heart Association)