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Regional differences in the arterial response to vasopressin: role of endothelial nitric oxide
Author(s) -
GarcíaVillalón Angel Luis,
García José Luis,
Fernández Nuria,
Monge Luis,
Gómez Bernardino,
Diéguez Godofredo
Publication year - 1996
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.1476-5381.1996.tb15613.x
Subject(s) - vasopressin , basilar artery , medicine , mesenteric arteries , vasopressin receptor , coronary arteries , contraction (grammar) , endocrinology , artery , cardiology , anesthesia , antagonist , receptor
1 . The isometric response to arginine‐vasopressin (10 −10 ‐10 −7 m ) was studied in 2 mm long rabbit arterial segments isolated from several vascular beds (cutaneous, pial, renal, coronary, muscular, mesenteric and pulmonary). 2 . Vasopressin induced contraction in central ear (cutaneous), basilar (pial), renal, coronary and saphenous (muscular) arteries, but had no effect in mesenteric and pulmonary arteries; the order of potency for the contraction was: ear > basilar > renal > coronary > saphenous arteries. 3 . Treatment with the blocker of nitric oxide synthesis N G ‐nitro‐L‐arginine methyl ester (L‐NAME; 10 −6 ‐10 −4 m ) increased significantly ( P < 0.05) the contraction to vasopressin in ear (148% of control), basilar (150% of control), renal (304% of control), coronary (437% of control) and saphenous (235% of control) arteries. Removal of the endothelium increased significantly ( P < 0.05) the contraction to vasopressin in basilar (138% of control), renal (253% of control), coronary (637% of control) and saphenous (662% of control) arteries, but not in ear artery. Mesenteric and pulmonary arteries in the presence of L‐NAME or after endothelium removal did not respond to vasopressin, as occurred in control conditions. 4 . The specific antagonist for V 1 vasopressin receptors d(CH 2 ) 5 Tyr(Me)AVP (3 × 10 −9 ‐10 −7 m ) was more potent (pA 2 = 9.3–10.1) than the antagonist for both V 1 and V 2 vasopressin receptors desGly‐d(CH 2 ) 5 ‐D‐Tyr(Et)ValAVP (10 −7 ‐10 −6 m ) (pA 2 = 7.4–8.4) to block the contraction to vasopressin of ear, basilar, renal and coronary arteries. 5 . The specific V 2 vasopressin agonist [deamino‐Cys 1 , D‐Arg 8 ]‐ vasopressin (desmopressin) (10 −10 ‐10 −7 m ) did not produce any effect in any of the arteries studied, with or without endothelium. 6 . In arteries precontracted with endothelin‐1, vasopressin or desmopressin did not produce relaxation. 7 . These results suggest: (a) most arterial beds studied (5 of 7) exhibit contraction to vasopressin with different intensity; (b) the vasoconstriction to this peptide is mediated mainly by stimulation of V 1 vasopressin receptors, and (c) endothelial nitric oxide may inhibit the vasoconstriction to this peptide, especially in coronary and renal vasculatures.