Somatostatin induces vasodilatation in the cat mesenteric artery via endothelium-derived nitric oxide and prostaglandins

• Published in: Pflügers Archiv Vol. 433; no. 4; pp. 536 - 538
• Main Authors: Dézsi, L, Dörnyei, G, Szentiványi, Jr, M, Tulassay, T, Monos, E
• Format: Journal Article
• Language: English
• Published: Germany 01-02-1997
• Subjects: Animals; Cats; Dose-Response Relationship, Drug; Female; Male; Mesenteric Arteries - drug effects; Nitric Oxide - physiology; Prostaglandins - physiology; Somatostatin - pharmacology; Vasodilation - drug effects
• ISSN: 0031-6768; 1432-2013
• DOI: 10.1007/s004240050310

Direct vascular effects of somatostatin (ST) were investigated in cat superior mesenteric artery (SMA) segments in vitro. Changes of outer diameter were measured at constant axial length and perfusion pressure. SMA segments in the resting state were not affected by ST, regardless of endothelial integrity. Noradrenaline-preconstricted SMA segments were dilated concentration-dependently by ST (EC50 10(-13) mol/l). At maximal dilatation (by 10(-11) mol/l ST) the preconstriction was diminished to 45 +/- 9% (P<0.001). Perfusion with Triton X-100, or NG-nitro-L-arginine nearly abolished the ST-induced dilatation, while indomethacin treatment partially suppressed it. We conclude that ST dilates preconstricted cat SMA segments mainly via the endothelial release of nitric oxide, and additionally via prostaglandins.