THROMBOXANE IN SEVERE HYPERTENSION

血栓素是花生四烯酸的代谢物，具有血小板聚集性 和血管收缩特性，并在以下情况下大量产生 血小板被刺激聚集起来。我们在YRONG中的初步发现 患有遗传性高血压的动物向我们暗示，有一种 血栓烷在高血压中的潜在作用。这让我们找到了 假设血栓素可能在高血压原中起重要作用 当存在血管损伤时，如严重高血压。增强版 血栓素在血管血小板沉积后的形成和 发生的纤维素样坏死可能会导致进一步的血压 抬高和血管损伤及相关并发症，如中风 和肾功能障碍。来验证我们的假设，即血栓烷是 与重度高血压患者的血压显著升高有关， 及其后遗症，将在两个SHRSP(一种遗传模型)中进行研究 完全结扎肾动脉之间的主动脉的大鼠(a 手术诱导的重度高血压模型)用血栓素A治疗 合成酶抑制剂、血栓素受体拮抗剂或化学稳定性 前列环素模拟物。水和电解质平衡，收缩动脉 治疗组和对照组的血压和尿液iTxB2均进行测定。 未经治疗的清醒动物。类似的研究将在#年进行 假手术组动物为主动脉结扎组和WKY组。血小板和 将进行肾功能研究以及血液测量。 两组患者血栓素和血管花生四烯酸代谢水平 已处理和未处理的动物。这些研究将评估 血栓素生成增加在重症高血压发病中的作用 及其后遗症，并可能提供对新模式的洞察 男性的降压治疗。

Thromboxane is a metabolite of arachidonic acid having platelet aggregatory and vasoconstrictor properties and is generated in large amounts when platelets are stimulated to aggregate. Our preliminary findings in young animals with genetic hypertension have suggested to us that there is an underlying role of thromboxane in hypertension. This has led us to hypothesize that thromboxane may play an important hypertensinogen role when vascular damage is present such as in severe hypertension. Enhanced thromboxane formation subsequent to the vascular platelet deposition and fibrinoid necrosis which occurs may lead to further blood pressure elevation and vascular damage and associated complications such as stroke and kidney dysfunction. To test our hypothesis that thromboxane is involved in the marked elevation of blood pressure in severe hypertension, and its sequelae, studies will be performed in both SHRSP (a genetic model) and rats with complete ligation of the aorta between the renal arteries (a surgically-induced model of severe hypertension) treated with thromboxane synthase inhibitors, thromboxane receptor antagonists or chemically stable prostacyclin mimetics. Water and electrolyte balance, systolic arterial pressure, and urinary iTxB2 will be measured in both treated and non-treated conscious animals. Similar studies will be carried out in animals which are sham operated for aortic ligation and WKY. Platelet and renal functional studies will be performed as well as measurements of blood levels of thromboxane and vascular arachidonic acid metabolism in both treated and non-treated animals. These studies will evaluate the role of enhanced thromboxane production in the development of severe hypertension and its sequelae and may provide insights into newer modes of antihypertensive therapy in man.