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1 Oregon Regional Primate Research Center, Beaverton 97006; and 2 The Dotter Interventional Institute, Oregon Health Sciences University, and 3 Dimera LLC, Portland, Oregon 97210
In the present
investigation, we test the hypothesis that progesterone can rapidly
relax, via a nongenomic mechanism, persistent flow occluding,
agonist-activated coronary artery (CA) vasospasm, and hyperreactive
vascular muscle cell (VMC) Ca2+ responses in ovariectomized
rhesus monkeys. CA vasospasm, induced by injection of 100 µM
serotonin and 1 µM U-46619 (5-HT+U; 1 ml/30 s), resulted in a
decrease in CA diameter (
) from 1.8 ± 0.2 to 0.3 ± 0.1 mm at the site of focal constriction. Injection of 100 ng progesterone
into the CA significantly relieved the severe vasoconstriction
(1.3 ± 0.2 mm) and reestablished distal flow in 3 min; the
preconstriction was completely restored in 8.2 ± 2.6 min
(n = 6). Similarly, cell impermeant albumin-conjugated progesterone, but not albumin-conjugated 17
-estradiol, decreased 5-HT+U stimulated VMC Ca2+ responses (250 ± 34% of
basal 30 min after stimulation) back to the prestimulation level
(113 ± 17% of basal) in 25 min (half time = 7 min). The
presence of a rapid vasodilator action of progesterone in the primate
CA and isolated VMC suggests its benefits in hormone replacement
therapy may also include nongenomic vascular relaxant actions.
vasospasm; angiography; ovarian steroids; nongenomic effects; low-dose progesterone; vascular muscle cell
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