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Center for Perinatal Biology, Department of Pharmacology, Loma Linda University School of Medicine, Loma Linda, California 92350
The effect of chronic hypoxia on free
intracellular Ca2+ concentration
([Ca2+]i)
and Ca2+ sensitivity of
myofilaments during agonist stimulation was examined in uterine
arteries obtained from normoxic and chronically hypoxic pregnant sheep
maintained at high altitude (3,820 m) for ~110 days. Smooth muscle
[Ca2+]i
was measured simultaneously with muscle contraction in the same intact
tissue. Whereas both KCl and 5-HT increased
[Ca2+]i
and tension simultaneously in the uterine artery, 5-HT produced significantly greater contractile tension (in g) than KCl at a given
amount of
[Ca2+]i
as indicated by the ratio of fura 2 fluorescence intensity induced by
excitation at 340 nm to that induced at 380 nm (29.8 ± 6.9 vs. 16.9 ± 4.0, P < 0.05).
Chronic hypoxia did not change KCl-induced contractions, nor did it
affect KCl-mediated increases in
[Ca2+]i.
In contrast, chronic hypoxia significantly inhibited 5-HT-induced contractions and decreased the 5-HT-stimulated increase in
[Ca2+]i
(pD2 7.46 ± 0.18 
6.86 ± 0.11, P < 0.05, where
pD2 is 
log half-maximal
effective concentration) in uterine arteries. In addition, the slope (g
tension/nM
[Ca2+]i)
of the 5-HT-mediated
[Ca2+]i-tension
relationship was significantly decreased in chronically hypoxic
arteries (0.024 ± 0.002 0.013 ± 0.001, P < 0.01). The results suggest that
chronic hypoxia suppresses agonist-mediated Ca2+ homeostasis in uterine
arteries by inhibiting Ca2+
mobilization and the agonist-enhanced
Ca2+ sensitivity of myofilaments.
uterine contractions; 5-hydroxytryptamine
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