OVLT lesion decreases basal arterial pressure and the chronic hypertensive response to AngII in rats on a high-salt diet.
OVLT lesion decreases basal arterial pressure and the chronic hypertensive response to AngII in rats on a high-salt diet.
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DOI：
10.1002/phy2.128
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发表时间：
2013-10
影响因子：
2.5
通讯作者：
Osborn, John W
中科院分区：
文献类型：
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作者：
Collister, John P;Olson, Marin K;Nahey, David B;Vieira, Alexandre A;Osborn, John W
我们已经报道，病变的终板血管器（OVLT）的平均动脉压（MAP）的基础水平没有影响，但废除了高血压的影响，血管紧张素II（AngII）在大鼠消耗正常盐饮食。这些结果表明，OVLT并不有助于正常盐摄入量的条件下，MAP的调节，但它是一个重要的脑血管紧张素II的高血压行动的网站。OVLT被认为是大脑中主要的钠传感器，高盐摄入会加剧AngII的高血压效应。因此，本研究的目的是研究OVLT在高盐饮食大鼠AngII诱导的高血压中的作用。雄性Sprague-Dawley大鼠接受假手术（Sham; n = 9）或OVLT病变（OVLTx; n = 8）手术，并接受高盐（2%NaCl）饮食。在三个对照日、10天AngII输注（10 ng/kg/min，静脉注射）、10天AngII输注（10 ng/kg/min，静脉注射）、10天AngII输注（10 ng/kg/min，静脉注射）、10天AngII输注（10 ng/kg/min，静脉注射）和10天AngII输注（10 ng/kg/min，静脉注射）期间通过无线电遥测测量MAP。还有三天的恢复期对照组MAP（97 ± 2 mmHg）显著低于假手术组（106 ± 1 mmHg）（P < 0.05）。此外，在OVLTx大鼠中，对AngII的慢性升压反应明显减弱。AngII治疗第10天，假手术组大鼠MAP升高58 ± 3 mmHg，而OVLTx组大鼠MAP升高40 ± 7 mmHg（P < 0.05）。我们的结论是：（1）OVLT调节高盐大鼠MAP的基础水平，（2）OVLT是大鼠AngII盐高血压发病机制的重要脑作用部位。由HL 076312支持。
We have reported that lesion of the organum vasculosum of the lamina terminalis (OVLT) has no effect on basal levels of mean arterial pressure (MAP) but abolishes the hypertensive effects of angiotensin II (AngII) in rats consuming a normal-salt diet. These results suggest that the OVLT does not contribute to regulation of MAP under conditions of normal salt intake, but it is an important brain site for the hypertensive actions of AngII. The OVLT has been proposed as a major sodium sensor in the brain and the hypertensive effects of AngII are exacerbated by high-salt intake. Therefore, the objective of this study was to investigate the role of the OVLT during AngII-induced hypertension in rats fed a high-salt diet. Male Sprague-Dawley rats underwent sham (Sham; n = 9) or OVLT lesion (OVLTx; n = 8) surgery and were placed on a high-salt (2% NaCl) diet. MAP was measured by radio telemetry during three control days, 10 days of AngII infusion (10 ng/kg/min, i.v.), and a 3-day recovery period. MAP was significantly lower in OVLTx (97 ± 2 mmHg) compared to Sham (106 ± 1 mmHg) rats during the control period (P < 0.05). Moreover, the chronic pressor response to AngII was markedly attenuated in OVLTx rats. MAP increased 58 ± 3 mmHg in Sham rats by Day 10 of AngII compared to a 40 ± 7 mmHg increase in OVLTx rats (P < 0.05). We conclude that (1) the OVLT regulates the basal levels of MAP in rats consuming a high-salt and (2) the OVLT is an important brain site of action for the pathogenesis of AngII-salt hypertension in the rat. Supported by HL076312.