Vagal reflex actions of atrial natriuretic peptide survive physiological but not pathological cardiac hypertrophy in rat

Abstract

Atrial natriuretic peptide (ANP) enhances cardiac vagal baroreflexes in normotensive animals. In spontaneously hypertensive rats (SHRs) this effect of ANP was absent. The reflex actions of ANP were preserved if hypertrophy was completely prevented in SHRs. However even a small amount of cardiac hypertrophy, with no hypertension, in SHRs was accompanied by a loss of the reflex bradycardic actions of ANP. In the present study, we investigated whether pathophysiological cardiac hypertrophy, induced by one-kidney, one-clip renovascular hypertension (1K-1C; n = 6), or physiological cardiac hypertrophy induced by chronic spontaneous, wheel-running exercise training (n = 7), similarly prevented vagal reflex actions of ANP. Cardiac baroreceptor-activated bradycardia was measured during rapid ramp increases (∼5 s) in blood pressure after bolus doses of methoxamine or vehicle in conscious, chronically instrumented rats during infusions of ANP (50 pmol kg −1 min −1 ). Compared with uninephrectomised control rats (n = 10), rats with 1K-1C had cardiac hypertrophy (∼55% increase in left ventricle:body weight (LV:BW) ratio; P < 0.05) and blunted vagal baroreflex gain (−0.93 ± 0.18 versus −0.50 ± 0.13 beats min −1 mmHg −1 ; P < 0.05). ANP did not augment baroreflex function in 1K-1C. Compared with their sedentary controls (n = 7), exercise-trained rats with cardiac hypertrophy (∼20% increase LV:BW ratio; P < 0.05) also had blunted ramp baroreflex bradycardia (−1.28 ± 0.23 versus −0.57 ± 0.09 beats min −1 mmHg −1 ; P < 0.05). In contrast, ANP more than doubled baroreflexbradycardiainexercise-trained rats(P < 0.05).The aetiologyof cardiachypertrophy therefore influenced whether ANP retained its vagal baroreflex enhancing properties.

Cardiovascular Autonomic Dysfunction in Chronic Kidney Disease: a Comprehensive Review

“…Studies suggest a critical role for ANP in inhibiting hypothalamic NE release [154,155] and enhancing cardiac vagal baroreflex and cardiopulmonary reflex function [156,157], suggesting a potential role for ANP in modulating autonomic function. In the SHR, ANPmediated facilitation of cardiac baroreflex is absent, indicating altered ANP-ANS interaction during disease [157,158]. The relationship between ANP and autonomic neuroregulation in health and disease is far from being completely understood, and clearly CKD is no exception.…”