Enhancement by vasopressin of adrenergic responses in human mesenteric arteries
Medina, P.; Noguera, I.; Aldasoro, M.; Vila, J.M.; Flor, B.; Lluch, S.
American Journal of Physiology 272(3 Pt 2): H1087-H1093
1997
ISSN/ISBN: 0002-9513 PMID: 9087579 Document Number: 478030
Vasopressin not only acts directly on blood vessels through V-1-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 times 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 times 10-6 to 5.0 times 10-7 M; P lt 0.05) without any alteration in maximal contractions. Vasopressin also potentiated KCl- and calcium-induced contractions. The V-1-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 (10-16 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 V-1-receptor stimulation. The amplifying effect of vasopressin on constrictor responses may be relevant in those clinical situations characterized by increased plasma vasopressin levels.