Neurons of the median preoptic nucleus contribute to chronic angiotensin II-salt induced hypertension in the rat.
Neurons of the median preoptic nucleus contribute to chronic angiotensin II-salt induced hypertension in the rat.
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上核前核的神经元有助于大鼠慢性血管紧张素II-盐诱导的高血压。
DOI：
10.14814/phy2.15551
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发表时间：
2022-12
影响因子：
2.5
通讯作者：
中科院分区：
文献类型：
--
作者：
实验旨在检验这样的假设：中位视前神经元 (MnPO) 对于高盐饮食大鼠对慢性血管紧张素 II (AngII) 的完全高血压反应是必要的。 MnPO 参与 AngII 的许多生理作用，主要作为 AngII 与心室周围器官（如终板血管器 (OVLT)）结合的下游核。我们之前已经证明，OVLT 损伤对 AngII 对食用高盐大鼠的慢性高血压作用有显着影响。此外，我们还发现，MnPO 损伤可减弱大鼠对长期静脉输注 AngII 的高血压反应。然而，MnPO 神经元或通道纤维是否有助于这种反应尚不清楚。雄性 Sprague Dawley 大鼠被随机分配至假手术组 (SHAM；n = 8) 或 MnPO 的鹅膏蕈酸损伤组 (MnPOx；n = 6)。在MnPOx组中，将200nl鹅膏菌酸的磷酸盐缓冲盐水(5μg/μl)注射到针对整个MnPO的3个预定坐标中的每一个中。恢复一周后，给大鼠安装无线电遥测压力传感器，随意提供 2.0% NaCl 饮食和蒸馏水，并再给予一周恢复时间。基线测量 3 天后，将微型渗透泵植入所有大鼠皮下，以 150 ng/kg/min 的速率施用 AngII。微型泵植入后 14 天进行血压测量。到 AngII 治疗第 7 天，两组的血压反应均趋于稳定，而 MnPOx 大鼠的高血压反应明显减弱（MnPOx，122±±6mmHg；SHAM，143±8mmHg）。这些结果支持这样的假设：MnPO 神经元参与介导 AngII 对高盐饮食大鼠的慢性高血压作用的中央通路。之前我们已经证明 MnPO 的电解损伤可以预防大鼠的慢性血管紧张素 II 高血压。目前，通过利用 MnPO 保留纤维的化学损伤，我们具体证明了 MnPO 神经元对于高盐饮食大鼠对血管紧张素 II 的完全高血压反应是必需的。
Experiments were designed to test the hypothesis that median preoptic (MnPO) neurons are necessary for the full hypertensive response to chronic angiotensin II (AngII) in rats consuming a high salt diet. The MnPO is implicated in many of the physiologic actions of AngII, primarily acting as a downstream nucleus to AngII binding at circumventricular organs such as the organum vasculosum of the lamina terminalis (OVLT). We have previously shown a prominent effect of lesion of the OVLT on the chronic hypertensive effects of AngII in rats consuming high salt. Additionally, we have shown that lesion of the MnPO attenuated the hypertensive response to chronic intravenous infusion of AngII in rats. However, whether MnPO neurons or fibers of passage contribute to this response is not clear. Male Sprague Dawley rats were randomly assigned to either sham (SHAM; n = 8) or ibotenic acid lesion of the MnPO (MnPOx; n = 6). In the MnPOx group, 200 nl of ibotenic acid in phosphate buffer saline (5 μg/μl) was injected into each of 3 predetermined coordinates targeted at the entire MnPO. After a week of recovery, rats were instrumented with radiotelemetric pressure transducers, provided 2.0% NaCl diet and distilled water ad libitum and given another week to recover. After 3 days of baseline measurements, osmotic minipumps were implanted subcutaneously in all rats for administration of AngII at a rate of 150 ng/kg/min. Blood pressure measurements were made for 14 days after minipump implantation. By day 7 of AngII treatment, blood pressure responses appeared to plateau in both groups while the hypertensive response was markedly attenuated in MnPOx rats (MnPOx, 122 ± 6 mmHg; SHAM, 143 ± 8 mmHg). These results support the hypothesis that neurons of the MnPO are involved in the central pathway mediating the chronic hypertensive effects of AngII in rats consuming a high salt diet. Previously we have shown electrolytic lesion of the MnPO prevents chronic angiotensin II hypertension in the rat. Currently, by utilizing chemical lesion of the MnPO sparing fibers of passage, we demonstrate specifically that neurons of the MnPO are necessary for the full hypertensive response to angiotensin II in rats consuming a high salt diet.
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影响因子：
2.7
作者：
Osborn JW;Fink GD
通讯作者：
Fink GD
影响因子：
--
作者：
GARDINER, TW;STRICKER, EM
通讯作者：
STRICKER, EM
影响因子：
4.1
作者：
MANGIAPANE, ML;THRASHER, TN;GANONG, WF
通讯作者：
GANONG, WF
DOI：
10.1161/hypertensionaha.108.127803
发表时间：
2009-08
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Adams JM;Bardgett ME;Stocker SD
通讯作者：
Stocker SD
影响因子：
4.1
作者：
MANGIAPANE, ML;SIMPSON, JB
通讯作者：
SIMPSON, JB