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Relaxation of human isolated mesenteric arteries by vasopressin and desmopressin
Author(s) -
Martinez M.C.,
Vila J.M.,
Aldasoro M.,
Medina P.,
Flor B.,
Lluch S.
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb17005.x
Subject(s) - vasopressin , desmopressin , mesenteric arteries , medicine , endocrinology , cardiology , artery
1 The effects of vasopressin and deamino‐8‐D‐arginine vasopressin (DDAVP, desmopressin) were studied in artery rings (0.8‐1 mm in external diameter) obtained from portions of human omentum during the course of abdominal operations (27 patients). 2 In arterial rings under resting tension, vasopressin produced concentration‐dependent, endothelium‐independent contractions with an EC 50 of 0.59 ± 0.12 n m . The V 1 antagonist d(CH 2 ) 5 Tyr(Me)AVP (1 μ) and the mixed V 1 ‐V 2 antagonist desGly‐d(CH 2 ) 5 D‐Tyr(Et)ValAVP (0.01 μ m ) displaced the control curve to vasopressin to the right in a parallel manner without differences in the maximal responses. In the presence of indomethacin (1 μ m ) the contractile response to vasopressin was significantly increased ( P < 0.01). 3 In precontracted arterial rings, previously treated with the V 1 antagonist, d(CH 2 ) 5 Tyr(Me)AVP (1 μ m ), vasopressin produced endothelium‐dependent relaxation. This relaxation was reduced significantly ( P < 0.05) by indomethacin (1 μ m ) and unaffected by the V 1 ‐V 2 receptor antagonist desGly‐d(CH 2 ) 5 D‐Tyr(Et)ValAVP (1 μ m ) or by N G ‐nitro‐L‐arginine methyl ester (L‐NAME, O.1 μ m ). 4 The selective V 2 receptor agonist, DDAVP, caused endothelium‐independent, concentration‐dependent relaxations in precontracted arterial rings that were inhibited by the mixed V 1 ‐V 2 receptor antagonist, but not by the V 1 receptor antagonist or by pretreatment with indomethacin or L‐NAME. 5 Results from this study suggest that vasopressin is primarily a constrictor of human mesenteric arteries by V 1 receptor stimulation; vasopressin causes dilatation only during V, receptor blockade. The relaxation appears to be mediated by the release of vasodilator prostaglandins from the endothelial cell layer and is independent of V 2 receptor stimulation or release of nitric oxide. In contrast, the relaxation induced by DDAVP is largely dependent on stimulation of V 2 receptors.