We investigated the hemodynamic effect of synthetic atrial natriuretic factor Auriculin A (ANF) and its influence on arterial baroreflex control of heart rate, systemic blood pressure, and perfuslon pressure in the hind limb (perfused at constant flow) in rabbits anesthetized withα-chloralose and urethane. The neural mechanisms underlying these effects were also studied. In the intact animal, a 45-minute constant infusion of ANF (2 μg/kg prime, 0.2 μg/kg/min) significantly reduced mean blood pressure and increased mean perfusion pressure, while heart rate did not change. Comparable data were obtained with lower (0.5 μg/kg + 0.05 μg/kg/min; 1 μg/kg + 0.1 μg/kg/min) or higher (4 μg/kg + 0.4 μg/kg/min; 8 μg/kg + 0.8 μg/kg/min) doses of ANF. In addition, ANF enhanced brady-cardic reflex responses to phenylephrine i.v. bolus administration, while it did not change baroreflex-mediated responses to nitroglycerin i.v. bolus administration and to 30-second bilateral carotid occlusion. The specificity of the influence of ANF on arterial baroreflex responses was confirmed by the observation that no significant change in reflex responses to phenylephrine or carotid occlusion was detectable during a comparable decrease in blood pressure induced by a constant infusion of nitroglycerin. Bilateral vagotomy prevented both the fall in blood pressure and the increase in perfusion pressure induced by ANF, while cholinergic blockade (atropine, 0.5 mg/kg i.v.) or adrenergic blockade (propranolol, 0.3 mg/kg i.v. + phentolamine, 0.3 mg/kg i.v.) did not modify the hemodynamic response to ANF observed in the Intact animal. The ANF-induced enhancement of the reflex bradycardic response to phenylephrine-induced rise in blood pressure was prevented by both vagotomy and atropine. In conclusion, our data suggest that in this experimental model an increase in parasympathetic tone is involved in the blood pressure lowering effect of synthetic ANF as well as in the potentiation of the reflex bradycardie response to phenylephrine-induced arterial baroreceptor loading caused by the peptide.