Cardiopulmonary mechanoreceptors and renin release in humans

We investigated the hemodynamic determinants of the reflex release of renin to changes in posture and blood volume distribution in healthy humans to determine the relative contribution of arterial and cardiopulmonary mechanoreceptors to the reflex release of renin under physiological circumstances. In the first experiments, we induced a selective decrease of right atrial pressure by inflation of cuffs around the thighs. Renin increased and returned toward baseline on decompression. The renin increase was neurogenic because plasma norepinephrine increased, the response was abolished by beta blockade, and renin did not increase in patients with denervated transplanted kidneys. The second experiments were performed with tilting and later filling a pressure suit to counteract the effect of tilting on gravitational pooling of the blood. Tilting elicited increases of renin and norepinephrine; filling the suit abolished these increases. Right atrial pressure fell with tilting and rose after filling the suit. Because the neck was elevated above the heart equally in both conditions, it is concluded that the increase and decrease of renin reflected decrease and increase of the stretch of cardiopulmonary receptors. The third experiments were performed by elevating the upper trunk with the legs remaining in a horizontal position (sitting). This caused a heart-to-neck pressure difference and an increased sympathetic outflow through unloading arterial baroreceptors. Norepinephrine increased but renin did not. Cardiopulmonary receptors exhibit an important influence on the reflex release of renin.