Capsaicin treatment attenuates the reflex excitation of sympathetic activity caused by chemical stimulation of intestinal afferent nerves.

Sympathetic reflexes elicited by stimulation of visceral receptors have been well investigated, but the central neurotransmitters mediating these reflexes are largely unknown. Therefore, experiments were done to evaluate the role of substance P in the central transmission of a sympathoexcitatory reflex elicited by stimulation of intestinal receptors. Activity of mesenteric and renal nerves was recorded electrophysiologically in chloralose/urethane-anesthetized rats. Stimulation of intestinal receptors by serosal application of 0.5-1.0 microgram bradykinin increased mesenteric nerve activity by 100 +/- 21%, renal nerve discharge by 33 +/- 9%, and systemic arterial pressure by 10 mm Hg. Chronic capsaicin treatment (cumulative dose 950 mg/kg) caused a 52% depletion of substance P-like immunoreactivity from dorsal root ganglia and a significant attenuation of these reflexes. Mesenteric nerve activity increased by 48 +/- 6% in the capsaicin-treated rats. Bradykinin did not cause significant changes in renal nerve activity or systemic arterial pressure in these rats. The excitation of mesenteric nerve activity was significantly greater than the increase in renal nerve activity int he untreated and capsaicin-treated rats; capsaicin treatment affected responses of both nerves similarly. Capsaicin treatment did not have generalized effects on sympathetic reflexes, as mesenteric and renal nerve activities were decreased by baroreceptor activation similarly in the untreated and capsaicin-treated rats. These results suggest that the central transmission of the reflex response to intestinal receptor stimulation is mediated in part by substance P or other capsaicin-sensitive peptides.