Hypoxia/reoxygenation selectively impairs 1b -adrenoceptor function
in small mesenteric arteries.
Gao, Hong, Ronald J. Korthuis, and Joseph N. Benoit.
Department of Physiology and Biophysics, Louisiana State,
University Medical Center, Shreveport, Louisiana 71130-3932 and
Department of Physiology, University of South Alabama, College of
Medicine, Mobile, Alabama 36688
APStracts 3:0107G, 1996.
The present study examined whether hypoxia/reoxygenation (H/R)
attenuates norepinephrine (NE) effectiveness in small arteries by
interfering with function of [alpha]1A and/or [alpha]1B-adrenoceptor
subtypes. Small mesenteric arteries ( nearly equal to 150 [mu]m) were
obtained from rats, mounted on a small vessel myograph in oxygenated
PSS and the relationship between NE concentrations and contractile
tension assessed. Hypoxia was induced by bubbling the vessels with
95% N2/5%CO2 for 15 min. Vessels were then reoxygenated for 30 min.
and NE responses reevaluated. Superoxide dismutase (SOD) and catalase
(CAT) were added to the PSS in one group of vessels to investigate
the role of reactive oxygen metabolites. In other groups, [alpha]1B
receptors were blocked with chloroethylclonidine and [alpha]1A
receptors were blocked with 5-methylurapidil or WB-4101 in order to
produce exclusive [alpha]1A or [alpha]1B responses to NE. H/R
decreased the NE pD2 (i.e., -log[EC50]) from 6.26 +/- 0.24 to 5.84
+/- 0.12 (p<0.05). SOD and CAT prevented the H/R induced
contractile dysfunction. [alpha]1A-receptor responses to NE were not
altered by H/R. In contrast, [alpha]1B-receptor responses were
significantly attenuated following H/R. The results indicate that
alterations in NE responsiveness following H/R are due to dysfunction
of the [alpha]1B signal transduction pathway.
Received 24 July 1995; accepted in final form 29 April 1996.
APS Manuscript Number G311-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 June 96