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Vol. 288, Issue 2, 407-413, February 1999
Department of Obstetrics and Gynecology, The University of Texas
Medical Branch, Galveston, Texas (V.J., Y.P.V., G.R.S., R.E.G.); and
Research Laboratories of Schering AG, Berlin, Germany (K.C.)
Corticotropin-releasing factor (CRF), a potent vasorelaxant, is
increased tremendously during human pregnancy. Placenta is the main
source for this increase. CRF is thought to be important in modulating
vascular resistance and uteroplacental blood flow during pregnancy.
Here we investigated pathways mediating a vasorelaxant effect of CRF in
the uterine artery. Two-millimeter segments of uterine artery (o.d.
300-400 µm) from day 18 pregnant rats were mounted in a small vessel
myograph and precontracted with norepinephrine, and relaxation
responses to CRF were studied. CRF relaxed the uterine artery in a
concentration-dependent manner. Relaxation of uterine artery by CRF was
abolished completely by 
-helical CRF 9-41 (CRF antagonist, 1 µmol)
and partially by removal of endothelium,
N
-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor, 0.1 mmol), 6-anilino-5,8-quinolinedione (guanylate cyclase
inhibitor, 10 µmol), or thiopental/miconazole (cytochrome P-450
inhibitors, 0.3 mmol/30 µmol), but remained unaffected by indomethacin (cyclo-oxygenase inhibitor, 10 µmol). Relaxation was
also inhibited when depolarizing solution (K+, 120 mmol)
was used for precontraction. In deendothelized preparations, relaxation
was not inhibited by
9-tetrahydro-2-furanyl-9H-purin-6-amine (adenylate
cyclase inhibitor, 0.2 mmol), glibenclamide (adenosine triphosphate-dependent K+ channel blocker, 10 µmol),
tetrabutyl ammonium (nonspecific K+ channel blocker, 1 mmol), nitrendipine (voltage-gated Ca++ channel blocker, 1 µmol), or when vessels were precontracted with depolarizing solution.
CRF causes vasorelaxation by receptor-operated, endothelium-dependent
and -independent pathways. The endothelium-dependent relaxation is
mediated by nitric oxide-cyclic guanosine monophosphate pathway and
endothelium-derived hyperpolarizing factor but not prostacyclin.
However, cyclic adenosine monophosphate, K+ channels, or
Ca++ channels are not involved in endothelium-independent
vasorelaxation by CRF.
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