OBJECTIVES: The aim of this study was to investigate characteristics of placental arteries capable of influencing vasomotor tone in the fetoplacental vascular bed. Contractile characteristics and endothelium-dependent and endothelium-independent relaxation were examined. STUDY DESIGN: By means of a small vessel myograph arteries of mean normalized internal diameter 353.22 +/- 13.14 microns were studied under isometric conditions. Contractile function was assessed with a variety of agonists, including angiotensin II, endothelin-1, the thromboxane mimetic U46619, prostaglandin E2, and prostaglandin F2 alpha. The effect of physiologic and supraphysiologic PO2 on vascular function was also examined. Relaxation was assessed in response to known endothelium-dependent vasodilators, including acetylcholine, bradykinin, histamine, and A23187 and to sodium nitroprusside (endothelium independent). The effect of indomethacin and the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester on contractile function was also evaluated. RESULTS: Sensitivity to sodium nitroprusside was reduced by a high PO2. U46619 was the most potent constrictor agonist studied. The response of precontracted arteries to known endothelium-dependent vasodilators was minimal, other than for histamine, which led to modest relaxation. The constrictor response to U46619 was increased in the presence of NG-nitro-L-arginine methyl ester. CONCLUSIONS: Oxygen tension may be an important determinant of relaxation in small placental arteries. Receptor-mediated release of endothelium-derived relaxing factor is not a major mechanism in the fetoplacental circulation.
OBJECTIVES: The aim of this study was to investigate characteristics of placental arteries capable of influencing vasomotor tone in the fetoplacental vascular bed. Contractile characteristics and endothelium-dependent and endothelium-independent relaxation were examined. STUDY DESIGN: By means of a small vessel myograph arteries of mean normalized internal diameter 353.22 +/- 13.14 microns were studied under isometric conditions. Contractile function was assessed with a variety of agonists, including angiotensin II, endothelin-1, the thromboxane mimetic U46619, prostaglandin E2, and prostaglandin F2 alpha. The effect of physiologic and supraphysiologic PO2 on vascular function was also examined. Relaxation was assessed in response to known endothelium-dependent vasodilators, including acetylcholine, bradykinin, histamine, and A23187 and to sodium nitroprusside (endothelium independent). The effect of indomethacin and the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester on contractile function was also evaluated. RESULTS: Sensitivity to sodium nitroprusside was reduced by a high PO2. U46619 was the most potent constrictor agonist studied. The response of precontracted arteries to known endothelium-dependent vasodilators was minimal, other than for histamine, which led to modest relaxation. The constrictor response to U46619 was increased in the presence of NG-nitro-L-arginine methyl ester. CONCLUSIONS:Oxygen tension may be an important determinant of relaxation in small placental arteries. Receptor-mediated release of endothelium-derived relaxing factor is not a major mechanism in the fetoplacental circulation.