Role of the Median Preoptic Nucleus in Arterial Pressure Regulation and Sodium and Water Homeostasis during High Dietary Salt Intake.
Role of the Median Preoptic Nucleus in Arterial Pressure Regulation and Sodium and Water Homeostasis during High Dietary Salt Intake.
复制标题
高盐摄入期间中位视前核在动脉压调节和钠和水稳态中的作用。
DOI：
10.1007/s11062-012-9307-8
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发表时间：
2012
期刊：
影响因子：
0.5
通讯作者：
Collister,JP
中科院分区：
文献类型：
--
作者：
Ployngam,T;Katz,SS;Collister,JP
血管紧张素II（ANG II）的渗透压和水平的变化是重要的外周信号，调节适当的中枢交感神经输出和维持正常的动脉压在高盐摄入。正中视前核（MnPO）接受来自穹窿下器（SFO）和终板血管器（OVLT）的相互输入，这些室周器官已被证明在渗透压和循环ANG II变化的多个中枢效应中是必要的，这些中枢效应旨在维持钠和水的稳态。因此，我们假设MnPO是慢性高盐饮食摄入期间通过改变渗透压和/或ANG II信号传导介导血压控制的中枢神经机制的重要组成部分。雄性Sprague-Dawley大鼠被随机分配至假手术组或电解损伤组。恢复7天后，分别用无线电遥测传感器和主动脉血流探针测量平均动脉压（MAP）+心率（HR）和心输出量（CO）。还植入股静脉导管以收集血液用于测量血浆渗透压和钠浓度以及血浆肾素活性。再给予大鼠10天恢复时间，然后进行为期28天的研究方案，包括7天的对照期（1.0% NaCl饮食），随后是14天的高盐（4.0% NaCl）和7天的恢复期（1.0% NaCl）。数据显示，尽管在高盐期间在MnPO-（n= 12）和假损伤（n= 8）大鼠中观察到MAP轻微增加，但在整个研究方案中，两组中的MAP、HR和CO之间没有显著差异。这些发现并不支持MnPO在高膳食盐摄入期间维持正常血压所必需的假设。然而，在高盐摄入的前4天，MnPO损伤大鼠的钠平衡低于假损伤大鼠。尽管这些结果可能部分由MnPO损伤大鼠中观察到的血浆高渗透压和高钠血症来解释，但它们也揭示了MnPO在慢性高膳食盐摄入期间中枢神经元控制肾钠处理的作用。
Changes in the osmolality and level of angiotensin II (ANG II) are important peripheral signals modulating appropriate central sympathetic output and maintaining normal arterial pressure during high salt intake. The median preoptic nucleus (MnPO) receives reciprocal inputs from thesubfornical organ(SFO) andorganum vasculosumof thelamina terminalis(OVLT), the circumventricular organs that have been shown to be necessary in multiple central effects of changes in the osmolality and circulating ANG II directed toward the maintenance of sodium and water homeostasis. We, therefore, hypothesized that the MnPO is a crucial part of the central neuronal mechanisms mediating the blood pressure control by altered osmolality and/or ANG II signaling during chronic high dietary salt intake. Male Sprague–Dawley rats were randomly assigned to either sham (operation) or electrolytic lesion of the MnPO. After a 7-day recovery, rats were instrumented with radiotelemetric transducers and aortic flow probes for measurement of the mean arterial pressure (MAP) + heart rate (HR) and cardiac output (CO), respectively. Femoral venous catheters were also implanted to collect blood for the measurements of plasma osmolality and sodium concentration, as well as plasma renin activity. Rats were given another 10 days to recover and then were subjected to a 28-day-long study protocol that included a 7-day control period (1.0% NaCl diet) followed by 14 days of high salt (4.0% NaCl), and a 7-day recovery period (1.0% NaCl). The data showed, that despite a slight increase in the MAP observed in both MnPO-(n= 12) and sham-lesioned (n= 8) rats during the high-salt period, there were no significant differences between the MAP, HR, and CO in the two groups throughout the study protocol. These findings do not support the hypothesis that the MnPO is necessary to maintain the normal blood pressure during high dietary salt intake. However, MnPO-lesioned rats showed less sodium balance than sham-lesioned rats during the first 4 days of high salt intake. Although these results may be explained partly by the plasma hyperosmolarity and hypernatremia observed in MnPO-lesioned rats, they also shed light on the role of the MnPO in central neuronal control of renal sodium handling during chronic high dietary salt intake.