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Chronic sympathetic denervation alters vascular smooth muscle contraction to endothelin receptor activation in mesenteric veins
Author(s) -
Li Melissa Wei,
Galligan James J,
Fink Gregory D
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1107
Subject(s) - splanchnic , medicine , splanchnic nerves , endocrinology , endothelin receptor , denervation , contraction (grammar) , vasoconstriction , hemodynamics , anesthesia , receptor , stimulation
A 5‐day iv infusion of the endothelin ETB receptor agonist sarafotoxin 6c (S6c) into normal rats causes a significant increase in mean arterial pressure (MAP). In vitro studies show that S6c relaxes most arteries but constricts veins. Therefore, venoconstriction may be an important mechanism of S6c‐induced hypertension. There is evidence showing that, besides causing direct venoconstriction, S6c may increase sympathetic nerve activity to the splanchnic vasculature, the main capacitance bed of the circulation. We have shown that when sympathetic innervation to the splanchnic region is removed by surgical excision of the celiac and superior mesenteric ganglia (celiac ganglionectomy; CGX) S6c‐induced hypertension is largely prevented. This study was to test the effects of CGX on in vitro vascular responses of splanchnic veins to ETB receptor activation. We hypothesized that chronic CGX might reduce vascular responsiveness to S6c, especially in veins. In one group of rats CGX was performed (n=4), while another group of rats were sham‐operated (SHAM; n=4). Mesenteric veins (MVs) and arteries (MAs) were extracted 10–14 days later. Vascular contractility to S6c and endothelin‐1 (ET‐1) was studied in vitro using video monitoring. CGX had no major effect on contraction of MAs to ET‐1. Contractions of MVs to S6c and ET‐1 were greater in CGX rats. These data indicate that CGX does not reduce but rather enhances the responses of MVs to S6c and ET‐1. Therefore, CGX does not prevent S6c‐induced hypertension by reducing vascular reactivity of the splanchnic vasculature to ETB receptor activation. (NIH P01HL70687)