ROLE OF PRESSOR PROSTANOIDS IN HYPERTENSION

这是一项研究血管紧张剂参与的建议 前列腺素在高血压前期机制中的作用。我们建议激活 非TXA2参与的二十烷基类化合物对血管TXA2/PGH2受体的影响 内皮依赖性血管收缩的介导性及其在血管内皮细胞中的作用 高血压的发病机制。以下目标将在#年实现 血压正常的大鼠和血管紧张素依赖和非依赖的大鼠 各种形式的高血压。1.血管紧张剂的特征 血管组织通过内皮依赖性释放二十烷基类化合物 机械装置。将使用生物测定和高效液相技术来定量和 根据色谱图、内皮依赖性、 合成所需的环氧合酶和血栓素合酶，以及 TXA2/PGH2受体在血管收缩中的作用 花生四烯酸从灌流液中释放的收缩物质 主动脉和肠系膜血管构筑。2.对刺激因素的研究 血管收缩药二十烷基类化合物的内皮依赖性释放。该版本 在不同药物刺激下的血管收缩物质二十烷基类化合物 在AIM 1.3中被检查。3.评价二十烷类化合物诱导的作用 TXA2/PGH2血管受体在激素介导下的激活 诱导血管收缩。我们将对比血管的反应 灌流和不灌流的离体血管中的各种激素 血栓素A2/前列环素受体在EDRF介导的血管抑制中的作用 放松一下。血管内皮依赖性血管紧张素转换酶的血管舒缩作用 独立代理人将在在场和缺席的情况下进行研究 TXA2/PGH2拮抗剂、TXA2在二十烷类化合物激活中的作用 TXA2/PGH2受体在血管紧张素依赖性高血压发病中的作用 独立形式的高血压。我们将对比……的发展 血栓素A_2/前列腺素H_2同时治疗和不同时治疗大鼠的高血压 拮抗剂，TXA2合成抑制剂，或两者联合使用。

This is a proposal to investigate the participation of vasoconstrictor prostanoids in prohypertensive mechanisms. We propose that activation of vascular TXA2/PGH2 receptors by eicosanoids other that TXA2 participates in the mediation of endothelium-dependent vasoconstriction and in the mechanisms of hypertension. The following aims will be addressed in normotensive rats and in rats with angiotensin dependent and independent forms of hypertension. 1. Characterization of the vasoconstrictor eicosanoids released from vascular tissues via endothelium-dependent mechanisms. Bioassay and HPLC techniques will be used to quantitate and characterize in terms of chromatographic profile, endothelium dependency, requirement of cyclooxygenase and thromboxane synthase for synthesis, and role of TXA2/PGH2 receptors in the implementation of vascular contraction, the contractile material released by arachidonic acid from the perfused aorta and mesenteric vasculature. 2. Investigation of the stimuli for endothelium-dependent release of vasoconstrictor eicosanoids. The release of vasoconstrictor eicosanoids during stimulation with various agents will be examined as in AIM 1. 3. Evaluation of the role of eicosanoid-induced activation of TXA2/PGH2 vascular receptors in the mediation of hormone- induced vasoconstriction. We will contrast the vascular responses to various hormones in isolated vasculatures perfused with and without TXA2/PGH2 vascular receptors in attenuation of EDRF-mediated vascular relaxation. The vasodilatory effect of endothelium-dependent and - independent agents will be studied in the presence and the absence of TXA2/PGH2 antagonists, TXA2 of the role played by eicosanoids that activate TXA2/PGH2 receptors in the development of angiotensin-dependent and - independent forms of hypertension. We will contrast the development of hypertension in rats with and without concurrent treatment with TXA2/PGH2 antagonists, TXA2 synthesis inhibitors, or both treatments combined.