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  • Title: Endothelium-dependent and -independent mechanisms of vasorelaxation by corticotropin-releasing factor in pregnant rat uterine artery.
    Author: Jain V, Vedernikov YP, Saade GR, Chwalisz K, Garfield RE.
    Journal: J Pharmacol Exp Ther; 1999 Feb; 288(2):407-13. PubMed ID: 9918539.
    Abstract:
    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 microm) 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 alpha-helical CRF 9-41 (CRF antagonist, 1 micromol) and partially by removal of endothelium, Nomega-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor, 0.1 mmol), 6-anilino-5,8-quinolinedione (guanylate cyclase inhibitor, 10 micromol), or thiopental/miconazole (cytochrome P-450 inhibitors, 0.3 mmol/30 micromol), but remained unaffected by indomethacin (cyclo-oxygenase inhibitor, 10 micromol). 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 micromol), tetrabutyl ammonium (nonspecific K+ channel blocker, 1 mmol), nitrendipine (voltage-gated Ca++ channel blocker, 1 micromol), 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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