Enhancement by vasopressin of adrenergic responses in human
mesenteric arteries.
Medina, Pascual, Inmaculada Noguera, Mart[stod]on Aldasoro, Jos[theta]
M. Vila, [angstrom]ablas Flor, and Salvador Lluch.
Department of Physiology, Research Unit and [angstrom]aDepartment
of Surgery, University of Valencia, 46010 Valencia, Spain
APStracts 3:0428H, 1996.
Vasopressin not only acts directly on blood vessels through V1
-receptor stimulation but may also 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 perivascular nerves in human mesenteric
arteries. Human mesenteric artery rings (3-3.5 mm long, 0.8-1.2 mm
external diameter) were obtained from 38 patients undergoing
abdominal operations. The artery rings were suspended in organ bath
chambers for isometric recording of tension. Vasopressin (3x10-11 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
(EC50 decreased from 2.2x10-6 M to 5.0x10-7 M; P<0.05) without
any alteration of maximal contractions. Vasopressin also potentiated
KCl-and calcium induced contractions. The V1 vasopressin antagonist
d(CH2)5Tyr(Me)AVP (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.
Received 16 July 1996; accepted in final form 20 September 1996.
APS Manuscript Number H635-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996