Relaxation effect of estradiol on different vasoconstrictor-induced responses in rat thoracal artery

This experiment was designed to compare the relaxant effect of estradiol on the contractions induced by 5-hydroxytryptamine, phenylephrine, and KCl in absence or presence of preincubation with the nitric oxide synthase inhibitor (NOS) N (omega)-nitro-L-arginine methylester (L-NAME). R at thoracic aorta contraction responses to vasoconstrictors were observed in the absence or presence of L-NAME. 17beta-Estradiol was added in increasing cumulative concentrations in the absence or presence of the L-NAME when the contractile response had reached a stable plateau. In the presence of L-NAME, 10(-6) M estradiol on precontracted 5-hydroxytryptamine rings caused significant relaxation in comparison with precontracted phenylephrine, KCl rings. In the presence of L-NAME, 10(-5) M and 10(-6) M estradiol doses on precontracted 5-hydroxytryptamine rings showed no significant difference in relaxation. The 10(-6) M, 10(-5) M, and 10(-4) M estradiol doses on precontracted phenylephrine caused concentration dependent relaxations. The results of this study show that acute vasorelaxation to 17beta-estradiol is largely mediated via NO-independent pathways by inhibiting Ca+2 influx from the extracellular space and Ca+2 released from intracellular stores.