Continuous inhibition of renin release in dogs by vagally innervated receptors in the cardiopulmonary region.

Abstract

Inhibition of the release of renin by vagal afferents from the heart and lungs was studied in 14 dogs with their aortic nerves cut and their carotid sinuses vascularly isolated. The release of renin from one kidney was calculated from the venous-arterial difference in plasma renin activity (radioimmunoassay) and the renal blood flow (electromagnetic flowmeter). Renin release was determined before and during temporary interruption of afferent vagal nerve traffic (bilateral cooling of the cervical vagi). With carotid sinus pressure maintained at 40 mm Hg, vagal cooling increased mean aortic blood pressure (24%), decreased renal blood flow (19%), and increased renin release (241%). With sinus pressure maintained at the mean aortic blood pressure existing during the control period, vagal cooling caused a lesser increase in mean aortic blood pressure (12%), little decrease in renal blood flow (7%), and a marked increase in renin release (522%). The changes in renal blood flow and renin release with vagal cooling were prevented by renal denervation. Thus, vagal afferents from the cardiopulmonary region exert a tonic restraint on the release of renin; this restraint occurs in circumstances in which these afferents cause little change in total renal blood flow.

The renin-angiotensin-aldosterone system in congestive failure in conscious dogs.

“…When a comparable drop in arterial pressure was induced by pulmonary artery constriction the rise in PRA was much less. Since the fall in arterial pressure was similar in both models (a 10-15- (25)(26)(27)(28). In the present experiments with TIVC constriction, right and left atrial pressures were reduced, whereas with pulmonary artery constriction right atrial pressure increased while left atrial pressure was decreased.…”

Chronic Vagus Nerve Stimulation Improves Autonomic Control and Attenuates Systemic Inflammation and Heart Failure Progression in a Canine High-Rate Pacing Model

“…VNS can also reduce activity in the renin-angiotensin-aldosterone system. 14,15 Inhibition of the renin-angiotensin-aldosterone system has been shown to be beneficial in HF treatment. 16,17 Indeed, chronic VNS has been demonstrated to prolong survival in a rat myocardial infarction model.…”

Renin response to stimulation of cardiopulmonary mechanoreceptors in man.

“…Stimulation of these receptors causes a general withdrawal of the sympathetic outflow, but the effect on renal sympathetic tone is most pronounced (3)(4)(5). It has been shown that cardiopulmonary receptors mediate renin release in animals (6)(7)(8)(9).…”