Abstract

In addition to projections through the vagus, cervical sympathetic, and aortic depressor nerves, baroreceptor afferents from the arch of the aorta are thought to rise through a superior laryngeal nerve (SLN) pathway in the rat. We evaluated this possibility, first, by determining the hemodynamic response to electrical stimulation of the SLN in anesthetized rats. Miniaturized pulsed-Doppler flow probes were placed on the right common iliac, superior mesenteric and left renal arteries. Stimulation of the SLN produced frequency-dependent (1–12 Hz) reductions in arterial pressure, heart rate and regional vascular resistance, with the greatest vasodilation occurring in the hindlimb. Right lumbar nerve transection selectively abolished the hindlimb response and attenuated the depressor effect of SLN stimulation. Mesenteric and renal vasodilation were markedly reduced by ganglionic blockade as was the reduction in arterial pressure and heart rate. Vagotomy alone and in combination with propranolol abolished bradycardia to SLN stimulation but had no effect on blood pressure or regional resistance responses, indicating that the reflex reduction in vascular resistance, rather than cardiac output, was the primary determinant of the depressor response. In a second group the pressure and heart rate responses to occlusion for 30 s of the bilateral common carotids (C), subdiaphragmatic aorta (A) and both vessels simultaneously (C + A) were evaluated before and after bilateral SLN transection. Transection of the SLN significantly potentiated the pressure increase produced by C and C + A occlusion. Bradycardia responses during C and A occlusions were converted to tachycardia following SLN transection. These data show that a strong baroreflex response may be elicited by both direct electrical and physiological stimulation of baroreceptor afferents in the SLN and suggest that the SLN may constitute a significant projection pathway for baroreceptors from the region of the aortic arch.

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