Atrial natriuretic peptide modulates baroreceptor reflex in spontaneously hypertensive rat.

Abstract

Our previous studies have suggested that atrial natriuretic peptide in the caudal nucleus tractus solitarii is involved in the centrally mediated regulation of blood pressure in the salt-sensitive spontaneously hypertensive rat (SHR). The current study tested the hypothesis that endogenous atrial natriuretic peptide in the caudal nucleus tractus solitarii participates in baroreceptor reflex control of heart rate in this hypertensive model. Salt-sensitive SHR and control Wistar-Kyoto (WKY) rats maintained on basal (1%) salt intake were studied. Arterial baroreceptor reflex-mediated changes in heart rate were recorded in conscious unrestrained rats during phenylephrine 55 fig), or artificial cerebrospinal fluid vehicle (50 nl) was microinjected into the caudal nucleus tractus solitarii. Phenylephrine infusion was then repeated and mean arterial pressure and heart rate were monitored as before. The slope of the heart rate/mean arterial pressure relation was significantly less (p<0.05) in the salt-sensitive SHR than in the WKY control, indicating that baroreceptor reflex control of heart rate was blunted in this hypertensive model. Microinjection of atrial natriuretic peptide into the caudal nucleus tractus solitarii further blunted (p<0.05) baroreceptor reflex control of heart rate in salt-sensitive SHR but not in WKY rats. In contrast, microinjection of the monoclonal antibody enhanced the sensitivity of baroreceptor reflex control of heart rate in salt-sensitive SHR but not in WKY rats. These data suggest that endogenous atrial natriuretic peptide in the caudal nucleus tractus solitarii modulates baroreceptor reflex control of heart rate in salt-sensitive SHR bat not in WKY rats. 1 -3 In an anesthetized normotensive rat preparation, systemic administration of ANP has been shown to reduce sympathetic tone by a mechanism that involves a vagal afferent pathway and is partially buffered by arterial baroreceptor reflexes. "3 Intravenous administration of ANP to anesthetized normotensive rats with intact arterial baroreceptors resulted in decreased sympathetic outflow accompanied by reductions in blood pressure and heart rate (HR). Sinoaortic denervation exaggerated these responses to intravenous ANP, whereas vagal cooling to 0°C reversibly abolished the Received January 3, 1992; accepted in revised form May 12, 1992. sympathoinhibitory effect of intravenous ANP, indicating that this reflexry mediated action was dependent on afferent C-fiber activity in the vagus nerves.2 Further, recent studies have shown that circulating ANP in doses that have little effect on either blood pressure or HR exerts a complex modulatory effect on arterial baroreceptor reflexes in conscious normotensive rats. -5 ANP markedly potentiated reflex bradycardia but attenuated reflex tachycardia in response to intravenous boluses of phenylephrine and nitroprusside, respectively; it did not modify the pressor response to carotid occlusion. 4 Mechanisms that have been adduced to account for these effects of ANP include sensitization of cardiop...

Atrial natriuretic peptide regulation of noradrenaline release in the anterior hypothalamic area of spontaneously hypertensive rats.

“…Whereas microinjection of ANP into AHA elicits a hypertensive response, ANP microinjection into the nucleus of the solitary tract causes hypotension and injection of an ANP antibody into the nucleus of the solitary tract causes hypertension (7,9). These effects in the nucleus of the solitary tract appear to relate to the ability of ANP to increase baroreflex responsiveness in SHR (38). The decrease in ANP in the nucleus of the solitary tract in SHR leads directly to a lack of activation of baroreflex feedback to the AHA, and thereby decreases the ability of AHA to inhibit the sympathetic nervous system.…”