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Vol. 288, Issue 3, 977-983, March 1999
Center for Perinatal Biology, The present study examined the effect of chronic hypoxia on coupling
efficiency of alpha-1 adrenoceptors to inositol
1,4,5-trisphosphate (InsP3) signaling in ovine uterine
artery. Chronic hypoxia did not change the time course of
InsP3 formation, but significantly decreased the potency
(pD2: 6.17 ± 0.09 
5.26 ± 0.12) and the maximal response (220.7 ± 21.7 147.7 ± 15.3 pmol/mg
protein) of norepinephrine-induced InsP3 synthesis. The
coupling efficiency of alpha-1 adrenoceptors to
InsP3 synthesis (picomoles InsP3 per femtomoles
receptor) was decreased 45% by chronic hypoxia. In addition,
simultaneous measurement of norepinephrine-induced contractions and
InsP3 synthesis indicated that for a given amount of
InsP3 generated, the contractile force of the uterine
artery was significantly less in chronically hypoxic than in control
tissues (0.27 ± 0.01 versus 0.35 ± 0.02 g tension/pmol
InsP3). InsP3 receptors were characterized
using radioligand binding techniques. Although the density of
InsP3 receptors was not changed by chronic hypoxia (Bmax: 325 ± 35 378 ± 18 fmol/mg protein), the dissociation constant
(Kd) of InsP3 to its receptors
was significantly increased (Kd: 5.20 ± 0.40 7.81 ± 0.34 nM). Analysis of InsP3
receptor occupancy-tension development relationship indicated no
difference in intrinsic ability of the InsP3-receptor
complex in eliciting contractions between the control and hypoxic
tissues. Our results suggest that chronic hypoxia attenuates coupling
efficiency of alpha-1 adrenoceptors to InsP3
synthesis in the uterine artery. In addition, the tissue contractile
sensitivity to InsP3 is reduced, which is mediated
predominantly by a decrease in InsP3 binding affinity to
InsP3 receptors.
0022-3565/99/2883-0977$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1999 by The American Society for Pharmacology and Experimental Therapeutics
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