title: Enhancement by vasopressin of adrenergic responses in human mesenteric arteries.
abstract: Vasopressin not only acts directly on blood vessels through V1-receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vitro and in vivo. The aim of the present study was to investigate whether subpressor concentrations of vasopressin could modify the constrictor responses to norepinephrine and electrical stimulation of the perivascular nerves in human mesenteric arteries. Human mesenteric artery rings (3-3.5 mm long, 0.8-1.2 mm OD) were obtained from 38 patients undergoing abdominal operations. The arterial rings were suspended in organ bath chambers for isometric recording of tension. Vasopressin (3 x 10(-11) M) enhanced the contractions elicited by electrical stimulation at 2, 4, and 8 Hz (by 100, 100, and 72%, respectively) and produced a leftward shift of the concentration-response curves to norepinephrine (half-maximal effective concentration decreased from 2.2 x 10(-6) to 5.0 x 10(-7) M; P < 0.05) without any alteration in maximal contractions. Vasopressin also potentiated KCl- and calcium-induced contractions. The V1-receptor antagonist 1-[beta-mercapto-beta,beta-cyclopentamethylenepropionic acid-2-O-methyl-tyrosine, 8-arginine]vasopressin (10(-6) M) prevented the potentiation evoked by vasopressin in all cases. The calcium antagonist nifedipine (10(-6) M) did not affect the potentiation of electrical stimulation and norepinephrine induced by vasopressin but abolished KCl-induced contractions. The results suggest that vasopressin, in addition to its direct vasoconstrictor effect, strongly potentiates the responses to adrenergic stimulation and KCl depolarization. Both the direct and indirect effects of vasopressin appear to be mediated by V1-receptor stimulation. The amplifying effect of vasopressin on constrictor responses may be relevant in those clinical situations characterized by increased plasma vasopressin levels.
authors.affiliation: Department of Physiology, University of Valencia, Spain.
authors.forename: P
authors.initials: P
authors.lastname: Medina
authors.forename: I
authors.initials: I
authors.lastname: Noguera
authors.forename: M
authors.initials: M
authors.lastname: Aldasoro
authors.forename: J M
authors.initials: JM
authors.lastname: Vila
authors.forename: B
authors.initials: B
authors.lastname: Flor
authors.forename: S
authors.initials: S
authors.lastname: Lluch
mesh_terms: D000328:Adult; D000368:Aged; D001127:Arginine Vasopressin / Q000031:analogs & derivatives / Q000494:pharmacology; D002122:Calcium Chloride / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D006727:Hormone Antagonists / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000502:physiology*; D008875:Middle Aged; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D009852:Omentum / Q000098:blood supply; D011189:Potassium Chloride / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology*
chemical_list: D006727:Hormone Antagonists; C089517:vasopressin, 1-(2-mercapto-2,2-(cyclopentamethylene)propionic acid)-2-(O-methyl)Tyr-8-Arg-; D014667:Vasopressins; D001127:Arginine Vasopressin; D011189:Potassium Chloride; D002122:Calcium Chloride; D009638:Norepinephrine