Effects of trout endothelin on the motility of gastrointestinal smooth muscle from the trout and rat

Citation
Yq. Wang et al., Effects of trout endothelin on the motility of gastrointestinal smooth muscle from the trout and rat, GEN C ENDOC, 123(2), 2001, pp. 156-162
Citations number
25
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
GENERAL AND COMPARATIVE ENDOCRINOLOGY
ISSN journal
00166480 → ACNP
Volume
123
Issue
2
Year of publication
2001
Pages
156 - 162
Database
ISI
SICI code
0016-6480(200108)123:2<156:EOTEOT>2.0.ZU;2-B
Abstract
Trout endothelin (ET), previously isolated from the kidney of the rainbow t rout Oncorhynchus mykiss, contains four amino acid substitutions at residue s 4-7 compared with rat ET-1. Trout ET produced sustained and concentration -dependent contractions of strips of longitudinal smooth muscle from trout stomach (pD(2) = 7.52 +/- 0.06) and proximal small intestine (pD(2) = 7.80 +/- 0.10) and from rat fundus (pD(2) = 7.78 +/- 0.14). Rat ET-1 was equipot ent with trout ET for contraction of rat fundus and 2- to 3-fold more poten t for contraction of trout gastrointestinal tissues. In contrast, rat ET-1 was 10- to 20-fold more potent than trout ET in constricting isolated rings of vascular tissue from trout efferent branchial artery and cardinal vein and from rat aorta (Y. Wang et al., 1999, Am.J. Pliysiol. 277, R1605-RI611) . It is known that the contractile effects of ET-1 on rat fundus are mediat ed through the ETB receptor and effects on the rat aorta are mediated throu gh the ETA receptor. We propose, therefore, that trout gastrointestinal tis sues express an ETB-type receptor that differentiates poorly between trout ET and rat ET-1, whereas trout vascular tissues express an ETA-type recepto r that is preferentially activated by rat ET-1. The rat ET-1-induced contra ctions of the trout gastrointestinal tissues are in part indirect, involvin g a serotoninergic neuronal pathway in the intestine and a noncholinergic, nonserotoninergic pathway in the stomach. (C) 2001 Academic Press.