Release of renin by the carotid baroreflex in anesthetized dogs. Role of cardiopulmonary vagal afferents and renal arterial pressure.

Abstract

SUMMARY In 3 of 10 anesthetized dogs with aortic nerves sectioned and renal arterial pressure maintained constant, reduction to 40 mm Hg of the pressure in the vascularly isolated carotid sinuses resulted in an increase in renin secretion. After section of the vagus nerves, carotid sinus hypotension resulted in an increase in renin secretion in 9 of the 10 dogs. Vagal nerve section in these 10 dogs with carotid sinuses vascularly isolated and maintained at a pressure equal to existing aortic pressure resulted in significant increases in basal levels of plasma renin activity and renin secretion. The increase in renin secretion found during carotid sinus hypotension in vagotomized dogs was totally or substantially inhibited when renal arterial pressure was not maintained constant but allowed to increase equally with systemic arterial pressure. The increase in renin secretion observed during carotid hypotension in vagotomized dogs with renal arterial pressure held constant was abolished by renal denervation. We conclude that the carotid baroreflex is involved in the neural control of renin release. However, a concomitant activation of cardiopulmonary receptors and/or a substantial rise in renal arterial pressure can suppress the reflex increase in the secretion of renin induced by carotid sinus hypotension. have shown that the release of renin in such diverse situations as suprarenal aortic stenosis, administration of the diuretic furosemide, and tilting to the upright position is dependent on neural mechanisms in considerable degree. In view of these observations, it is surprising to find disagreement regarding the role of the carotid baroreflex in the control of renin secretion. Three studies"*" 12 reported an increase in renin secretion during carotid occlusion and three studies 13 " 15 reported that renin secretion was not affected by changes in carotid sinus pressure. IN THE LAST FEW YEARS increasing attention hasIn a recent study it was shown that, when the carotid sinus was free to exert its buffering influence, complete interruption of afferent vagal nerve traffic from cardiopulmonary receptors did not result in an increase in renin secretion in 17 of 20 dogs. 16 Because it has been shown that the inhibitory influence of vagally innervated cardio- pulmonary receptors becomes more pronounced as that of the carotid baroreceptors is reduced," it seemed possible that this interaction between the two receptor systems might act to inhibit the release of renin during carotid sinus hypotension. The following studies were carried out to investigate this question. MethodsDogs weighing 16-20 kg were maintained on a daily intake of 65 mEq of Na + and 55 mEq of K + for 5 days before study. Anesthesia was induced with sodium thiopental (30 mg/kg, intravenously) followed by a-chloralose (80 mg/kg dissolved in 5% dextrose in water and administered intravenously). Supplemental doses of chloralose (5-10 mg/kg) were given hourly. Gallamine triethiodide (Flaxedil; 3 mg/kg, iv) was used to obtain muscle relaxation during the su...

Role of cardiovascular receptors on the neural regulation of renin release in normal men.

“…This increased pressure may have had an effect on renal or other arterial baroreceptors and thereby could have counterbalanced the effect of carotid sinus unloading on renin release. 2 Similar problems have been encountered by Mancia et al 22 with the use of a pneumatic neck chamber to unload carotid baroreceptors. In spite of substantial relfex activation, the plasma renin did not increase.…”

“…The blood pressure increase elicited by the unloading of arterial baroreceptors tends to offset the influence that arterial baroreceptors may have on renin release. Thus, Jarecki et al 2 had to maintain a constant renal perfusion pressure, cut the vagal afferents, and only then were able to show that alterations of carotid sinus pressure cause variations of renin release. This important study clarifies the potential influence that arterial baroreceptors have on reflex renin release, but does not explain the role of these receptors under physiologic circumstances.…”

“…Apparently, as Jarecki et al 2 did, one has to create highly artificial experimental conditions and prevent the naturally occurring pressure rise to show the effect of arterial baroreceptors on renin release. The practical message from our study and those of Mancia et al 9 is that, because of pressure changes, such an influence on renin release could not be shown in intact human beings.…”