EFFECT OF PREGNANCY UPON ENDOTHELIAL FUNCTION

血管内皮细胞调节血管平滑肌对内源性的反应 收缩物质通过代谢失活或通过 释放自己的血管活性物质(S)。通常情况下，会有一种微妙的 扩张和收缩之间的平衡。这种平衡在一些国家失去了 疾病状态。关于怀孕对健康的影响我们知之甚少。 内皮功能。怀孕与体重减少有关 对许多内源性收缩药敏感，血管减少 阻力，以及增加的心输出量的重新分配。这个 直接导致这些变化的刺激因素尚不清楚，而且 不知道它们是否有关联。怀孕与增加有关 子宫动脉内皮源性松弛因子(EDRF)。这个 去甲肾上腺素引起的子宫动脉收缩反应减弱 妊娠是次于EDRF的。 我们假设内皮或具有生殖功能的重要血管 在怀孕期间，床上的荷尔蒙会发生变化，从而增强补品。 刺激内皮扩张剂的释放，减少血管内皮细胞的释放 蟒蛇。我们进一步假设，这些变化是直接 负责将母体心输出量重新分配到器官 对成功怀孕和减少血管病变至关重要 对缩宫剂敏感。 具体目标1：确定NO-EDRF释放的时间进程和 妊娠期EDRF升高的内皮机制。 具体目标2：确定补药或刺激释放 NO-EDRF是雌激素依赖的。 具体目标3：确定ACh-EDRF活性增加 在怀孕期间或在雌激素治疗后， 毒鼠强受体状态。 具体目标4：确定怀孕对 血管内皮衍生的血管活性因子在不同的动脉和静脉中不同 从“生殖”和“非生殖”器官中分离出来。

The endothelium modulates the vascular smooth muscle response to endogenous constrictor substances by either inactivating them metabolically or by releasing its own vasoactive agent(s). Normally, there is a delicate balance between dilators and constrictors. This balance is lost in some disease states. Little is known about the effect of pregnancy upon endothelial function. Pregnancy is associated with a reduction in sensitivity to many endogenous constrictors, a decrease in vascular resistance, and a redistribution of an increased cardiac output. The stimuli directly responsible for these alterations are unclear and it is unknown if they are linked. Pregnancy is associated with increased endothelium derived relaxing factor (EDRF) in the uterine artery. The decreased uterine artery contractile responses to norepinephrine during pregnancy are secondary to EDRF. We hypothesize that the endothelium or reproductively important vascular beds are hormonally altered during pregnancy resulting in enhanced tonic and stimulated release of endothelial dilators and decreased release of constrictors. We further hypothesize that these changes are directly responsible for the redistribution of maternal cardiac output to organs crucial for a successful pregnancy and the reduction in vascular sensitivity to constrictor agents. Specific Aim 1: To determine the time course of NO-EDRF release and endothelial mechanisms which mediate the increase in EDRF during pregnancy. Specific Aim 2: To determine whether the tonic or stimulated release of NO-EDRF is estrogen dependent. Specific Aim 3: To determine whether the increased ACh-EDRF activity during pregnancy or after estrogen pretreatment parallels a change in muscarinic receptor status. Specific Aim 4: To determine whether the effect of pregnancy upon endothelium-derived vasoactive factors differs among arteries and veins from "reproductive" and "nonreproductive" organs.