Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats.
Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats.
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DOI：
10.1152/ajpregu.00622.2005
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发表时间：
2006-07
期刊：
影响因子：
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通讯作者：
Patrick J Mueller;Margaret J. Sullivan;R. R. Grindstaff-R.;J. Thomas Cunningham;E. Hasser
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作者：
Patrick J Mueller;Margaret J. Sullivan;R. R. Grindstaff-R.;J. Thomas Cunningham;E. Hasser
心血管失调发生在航天飞行后的宇航员或卧床休息的个体中。其特征在于立位不耐受的发生率增加。立位不耐受的机制可能是多因素的，可能包括血容量不足、自主神经功能障碍以及血管和心脏改变。动脉压力感受性反射是机体对立位应激反应的重要代偿机制。在以前的研究中，我们证明了动脉压力感受性反射介导的交感神经兴奋在后肢卸载（HU）大鼠，心血管失调的模型中是钝化的。动脉压力感受器反射也有助于调节血管活性激素，包括加压素和血管紧张素II。在本研究中，我们测试的假设，神经体液反应低血压也衰减后，大鼠后肢卸载14天。为了检验这一假设，在清醒的HU和对照大鼠中分别给予血管扩张剂二氮嗪（15或25 mg/kg）或生理盐水（0.9%）以产生低血压或对照条件。收集血浆样品并测定血管加压素和血浆肾素活性（PRA）。与生理盐水对照组相比，二氮嗪（25 mg/kg）可显著增加血管加压素和PRA。HU大鼠表现出显着较高水平的加压素在休息和加压素水平的增加，在低血压过程中增强后肢卸载。无论是休息，也不悬吊诱导PRA被后肢卸载改变。这些数据表明，虽然压力反射介导的交感神经兴奋是由后肢卸载钝化，加压素释放增强和加压素诱导的PRA是不受影响的。增加循环加压素可能用于补偿由后肢卸荷产生的交感神经活动的压力反射调节的钝化，或者实际上可能有助于它。
Cardiovascular deconditioning occurs in astronauts after spaceflight or in individuals subjected to bed rest. It is characterized by an increased incidence of orthostatic intolerance. The mechanisms responsible for orthostatic intolerance are likely multifactorial and may include hypovolemia, autonomic dysfunction, and vascular and cardiac alterations. The arterial baroreflex is an important compensatory mechanism in the response to an orthostatic stress. In a previous study, we demonstrated that arterial baroreflex mediated sympathoexcitation was blunted in hindlimb-unloaded (HU) rats, a model of cardiovascular deconditioning. The arterial baroreflex also contributes to the regulation of vasoactive hormones including vasopressin and angiotensin II. In the present study, we tested the hypothesis that the neurohumoral response to hypotension is also attenuated in rats after 14 days of hindlimb unloading. To test this hypothesis, the vasodilator diazoxide (15 or 25 mg/kg) or saline (0.9%) was administered to produce hypotension or control conditions, respectively, in conscious HU and control rats. Plasma samples were collected and assayed for vasopressin and plasma renin activity (PRA). Diazoxide (25 mg/kg) produced significant increases in vasopressin and PRA compared with saline controls. HU rats exhibited significantly higher levels of vasopressin at rest and the increase in vasopressin levels during hypotension was enhanced by hindlimb unloading. Neither resting nor hypotension-induced PRA was altered by hindlimb unloading. These data suggest that although baroreflex-mediated sympathoexcitation is blunted by hindlimb unloading, hypotension-induced vasopressin release is enhanced and hypotension-induced PRA is unaffected. Increased circulating vasopressin may serve to compensate for blunted baroreflex regulation of sympathetic nervous activity produced by hindlimb unloading or may actually contribute to it.