REGIONAL DIFFERENCES IN THE ARTERIAL RESPONSE TO VASOPRESSIN - ROLE OF ENDOTHELIAL NITRIC-OXIDE

1 The isometric response to arginine-vasopressin (10(-10)-10(-7) M) wa s 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 (cuta neous), basilar (pial), renal, coronary and saphenous (muscular) arter ies, 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 syn thesis N-G-nitro-L-arginine methyl ester (L-NAME; 10(-6)-10(-4) M) inc reased significantly (P<0.05) the contraction to vasopressin in ear (1 48% of control), basilar (150% of control), renal (304% of control), c oronary (437% of control) and saphenous (235% of control) arteries. Re moval of the endothelium increased significantly (P<0.05) the contract ion to vasopressin in basilar (138% of control), renal (253% of contro l), coronary (637% of control) and saphenous (662% of control) arterie s, but not in ear artery. Mesenteric and pulmonary arteries in the pre sence of L-NAME or after endothelium removal did not respond to vasopr essin, as occurred in control conditions. 4 The specific antagonist fo r V-1 vasopressin receptors d(CH2)(5)Tyr(Me)AVP (3 x 10(-9)-10(-7) M) was more potent (pA(2) = 9.3-10.1) than the antagonist for both V-1 an d V-2 vasopressin receptors desGly-d(CH2)(5)-D-Tyr(Et)valAVP (10(-7)-1 0(-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 vasopres sin agonist [deamino-Cys(1), D-Arg(8)]-vasopressin (desmopressin) (10( -10) 10(-7) M) did not produce any effect in any of the arteries studi ed, with or without endothelium. 6 In arteries precontracted with endo thelin-1, vasopressin or desmopressin did not produce relaxation. 7 Th ese results suggest: (a) most arterial beds studied (5 of 7) exhibit c ontraction to vasopressin with different intensity; (b) the vasoconstr iction to this peptide is mediated mainly by stimulation of V-1 vasopr essin receptors, and (c) endothelial nitric oxide may inhibit the vaso constriction to this peptide, especially in coronary and renal vascula tures.