Sympathetic modulation of rabbit aortic baroreceptors in vitro.

Previous studies indicate that sympathetic efferent nerves to the carotid sinus can modulate carotid sinus baroreceptor (BR) activity. There are, however, no studies that demonstrate this in the aortic arch. Since application of exogenous norepinephrine to the aortic arch can alter BR activity, we examined whether electrically stimulating the efferent innervation would likewise be effective. We used an in vitro preparation from anesthetized rabbits. This consisted of the aortic arch and sections of the aortic afferent and sympathetic efferent nerves. The aorta was perfused at a constant pulseless pressure set 10-15 mmHg above BR pressure threshold, and aortic diameter was measured with a photoelectric device. We electrically stimulated the efferent innervation with 1-ms duration constant-voltage pulses, while simultaneously recording aortic pressure, diameter, and BR discharge. In 12 of 18 BRs, discharge decreased with vasoconstriction and subsequently recovered with vasorelaxation. This BR inhibition was blocked when constriction was prevented with the alpha-adrenergic antagonist prazosin (10(-6) M). In the remaining six BRs, discharge increased in five units and remained constant in one unit; however, the excitation occurred only during and a few seconds after the stimulus period. Discharge then fell below control while aortic constriction persisted and subsequently increased back to control with aortic relaxation. In this second group of fibers, treatment with the smooth muscle relaxant sodium nitroprusside (10(-6) M) prevented BR inhibition but not excitation. Lastly, BR responses were eliminated if the efferent nerve was crushed but not cut, indicating that the sensory endings were not activated directly by electrotonic current spread.(ABSTRACT TRUNCATED AT 250 WORDS)