Activation of vagal depressor reflexes by atriopeptins inhibits renal sympathetic nerve activity

TLDR

Atrial natriuretic factor lowers arterial pressure without inducing reflex tachycardia, possibly due to stimulation of cardiac‑sensory receptors that activate vagal afferents. The study tests whether atriopeptins inhibit sympathetic nerve activity by activating vagal afferents. Renal sympathetic nerve activity, heart rate, and arterial pressure were recorded in anesthetized rats during injections of APII and APIII, with comparisons among intact, sinoaortic‑denervated, and denervated‑plus‑bilateral‑vagotomy conditions. APII lowered arterial pressure without raising renal sympathetic nerve activity or heart rate, whereas a comparable hypotensive agent increased these parameters; in denervated rats APIII still reduced MAP and suppressed renal SNA, an effect eliminated by vagotomy, indicating that atriopeptins activate vagal afferents to inhibit sympathetic outflow and heart rate.

Abstract

Atrial natriuretic factor decreases arterial pressure but the hypotensive response is not accompanied by the expected reflex tachycardia. The absence of reflex tachycardia might reflect a stimulating effect of atrial natriuretic factor [atriopeptins (AP)] on cardiac-sensory receptors with vagal afferents. To test the hypothesis that AP inhibit sympathetic nerve activity by activating vagal afferents we measured changes in renal sympathetic nerve activity (SNA), heart rate, and arterial pressure during injection of APII and APIII in anesthetized Sprague-Dawley rats in the intact state, after sinoaortic denervation, and after sinoaortic denervation plus bilateral vagotomy. In intact, anesthetized rats APIII (50 micrograms/kg) lowered mean arterial pressure [-31 +/- 8 (SE) mmHg] without the expected reflex increase in renal SNA and heart rate. In contrast, infusion of sodium nitroprusside in a dose that produced a similar decrease in mean arterial pressure (-29 +/- 9 mmHg) evoked a significant increase in renal SNA (+38 +/- 8%) and heart rate (+17 +/- 5 beats/min). In rats with sinoaortic denervation, APIII induced a greater fall in mean arterial pressure (-44 +/- 8 mmHg). This hypotensive response was associated with a decrease in renal SNA (-26 +/- 2%) that was abolished by bilateral vagotomy. Atropine did not attenuate the decrease in renal SNA with APIII. We conclude that APII and APIII increase the activity of vagal afferents and thereby inhibit the increases in renal SNA and heart rate, which would be expected to result from the fall in arterial pressure. We speculate that this action might facilitate reflexly the renal vasodilator and natriuretic actions of APs.