Capsaicin-Sensitive Nerves Modulate Reactive Hyperemia in Rat Gut

Abstract

Reactive hyperemia (RH) is a local, vascular response that occurs following release from mechanical occlusion of an artery, with restoration of intra-arterial pressure. The mechanism of this postocclusion hyperemia in the gut has not been identified, although metabolic, myogenic, and neurogenic mediators of this response have been proposed. The present study was conducted to evaluate a possible modulatory role for sensory innervation of the intestinal vasculature in RH, using acute and chronic treatment with capsaicin applied in different ways. In anesthetized rats, the velocity of flowing blood in the gut was determined continuously with a pulsed Doppler velocimeter, and arterial pressure was determined with a transducer. The increase in calculated intestinal vascular conductance at the height of RH (Ch), the excess volume of blood accumulating during RH, and the duration of the hyperemia were also used to quantify RH after occluding the anterior mesenteric artery for 30, 60, and 120 sec. In the initial control group of rats, the maximal increases in the velocity of flowing blood during RH were 61 +/- 4%, 90 +/- 7%, and 129 +/- 10% of control, conductances were increased to 192 +/- 5%, 222 +/- 12%, and 267 +/- 15% of control, volumes were 3.5 +/- 0.6 ml, 7.2 +/- 0.4 ml, and 16.2 +/- 1.8 ml, and durations of hyperemia were 78 +/- 5 sec, 93 +/- 6 sec, and 178 +/- 7 sec, respectively, after each elapsed period of occlusion. Acute treatment with periarterial capsaicin significantly decreased peak conductances in RH by 15-35% for all occlusions tested and reduced both volume and duration values. Rats treated with capsaicin in neonatal life exhibited reduced Ch values, as did adult rats treated chronically with capsaicin. Both periarterial and intrajejunal treatment with capsaicin decreased the duration of RH. Hexamethonium increased both Ch and the duration of RH and tended to reverse reductions in these parameters caused by capsaicin. These results suggest that sensory innervation of the intestinal vasculature exerts a modulatory influence in the regulation of intestinal RH.

The Gastrointestinal Circulation: Physiology and Pathophysiology

“…Studies using this approach have revealed a role for sensory nerves in the functional intestinal hyperemia elicited by oleic acid; however, this response (discussed in more detail in the section below dealing with postprandial intestinal hyperemia) is complicated by the mucosal injury that may be induced by oleic acid (298,373,514). Capsaicin desensitization can also substantially blunt the reactive hyperemic response in the intestine (223), autoregulatory escape in the stomach (306) and intestine (403), as well as the myogenic response of mesenteric arterioles (432). The experimental challenges used to elicit these vascular responses are rather innocuous and thus activation of sensory fibers cannot be attributed to mucosal irritation or injury.…”

Peptidergic sensory neurons in the control of vascular functions: Mechanisms and significance in the cutaneous and splanchnic vascular beds

“…Defunctionalization of capsaicin-sensitive afferent neurons has been found to reduce postocclusive hyperaemia in the rat hindleg (Lembeck and Donner 1981a) and gut (Hottenstein et al 1992), whereas in the pig postocclusive vasodilatation in skin, skeletal muscle and heart is independent of capsaicin-sensitive afferent neurons (Franco-Cereceda and Lundberg 1989). In contrast, the cutaneous hyperaemia in the human forearm skin evoked by exercise is blunted 24 h after intradermai injection of capsaicin (Kurozawa et al 1991).…”