Acetylcholine-induced relaxation in human uterine arteries is mediated by endothelial nitric oxide formation.
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Hypothesis-generating for NO-mediated uterine artery relaxation; leaves open translation to human reproductive outcomes.
The effect of acetylcholine on the isolated human uterine artery rings was investigated. Acetylcholine (10(-10) M to 6 x 10(-5) M) induced concentration- and endothelium-dependent relaxation (pD2 = 7.4 +/- 0.02, maximal response was 77.5 +/- 6.3% of relaxation induced by papaverine at 3 x 10(-4) M) of the pre-contracted arterial segments. Indomethacin (10(-5) M), diethylcarbamazine (10(-4) M) and tetra-ethylammonium (3 x 10(-4) M) had no effects on acetylcholine-evoked relaxation. Methylene blue (10(-5) M) and NG-monomethyl-L-arginine (L-NMMA) (3 x 10(-6) to 3 x 10(-5) M) antagonized relaxation induced by acetylcholine. The inhibition of endothelium-dependent relaxation by L-NMMA (10(-5) M) was reversed by L-arginine (10(-5) M) but not by D-arginine (10(-4) M). It is concluded that in uterine artery acetylcholine induces endothelium-dependent relaxation of isolated uterine artery is probably mediated via endothelial nitric oxide formation.
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Jovanovié et al. (1994) studied this question.
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