Intrarenal transport and vasoactive substances in hypertension

Intrarenal transport and vasoactive substances in hypertension
复制标题

DOI:
10.1161/hy09t1.093361
复制
发表时间:
2001-09-01
期刊:
影响因子:
8.3
通讯作者:
Garvin, JL
Garvin, JL
中科院分区:
医学1区
文献类型:
--
作者:
Ortiz, PA;Garvin, JL

文献摘要

被引文献

相似文献

血压受几种血管活性因子的影响,这些因子也调节肾单位转运。肾单位对盐重吸收的调节失衡会导致高血压。在自发性高血压大鼠(SHR)中,近端肾单位对多巴胺和血管紧张素II的反应分别减弱和增强。这部分解释了为什么SHR的近端小管比正常血压对照组吸收更多的盐和水。在Dahl盐敏感大鼠中,NO信号传导的缺陷和花生四烯酸/细胞色素P450途径的改变与粗升支增加的盐重吸收有关。在其他动物模型中,如醋酸去氧皮质酮(DOCA)盐大鼠,高血压的发展是由于诱导的激素失衡。通过模仿醛固酮的作用,DOCA刺激集合管中的钠重吸收,引起盐和液体潴留。因此,该模型类似于由盐皮质激素转运的异常调节引起的人类高血压的遗传形式,例如明显的盐皮质激素过量和糖皮质激素可治疗的醛固酮增多症。总之,这些发现表明血管活性化合物在调节肾单位转运和控制血压中的重要性。然而,重要的问题,体液控制的肾单位运输及其在高血压的影响仍然没有答案,在这些领域的深入研究是必要的。
Blood pressure is influenced by several vasoactive factors that also regulate nephron transport. An imbalance in regulation of salt reabsorption by the nephron contributes to hypertension. In the spontaneously hypertensive rat (SHR), the responses to dopamine and angiotensin II in the proximal nephron are diminished and enhanced, respectively. This partially explains why the proximal tubule of SHR absorbs more salt and water than that of normotensive controls. In the Dahl salt-sensitive rat, defects in NO signaling and alterations in the arachidonic acid/cytochrome P450 pathways are associated with increased salt reabsorption by the thick ascending limb. In other animal models, such as the deoxycorticosterone acetate (DOCA)-salt rat, hypertension develops as the result of an induced hormonal imbalance. By mimicking the effects of aldosterone, DOCA stimulates sodium reabsorption in the collecting ducts, causing salt and fluid retention. Thus, this model is similar to inherited forms of human hypertension caused by abnormal regulation of transport by mineralocorticoids, such as apparent mineralocorticoid excess and glucocorticoid-remediable aldosteronism. Overall, these findings demonstrate the significance of vasoactive compounds in regulating nephron transport and controlling blood pressure. However, important questions regarding humoral control of nephron transport and its implications in hypertension remain unanswered, and intensive research in these areas is required.