Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats.
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats.
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在麻醉的血管紧张素 II-盐高血压大鼠中，RVLM 血管运动神经元的放电不增加。
DOI：
10.1152/ajpheart.00657.2013
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Toney,GlennM
中科院分区：
文献类型：
--
作者：
Pedrino,GustavoR;Calderon,AlfredoS;Andrade,MaryAnn;Cravo,SergioL;Toney,GlennM
延髓吻侧腹外侧（RVLM）神经元是产生和调节交感神经活动（SNA）的关键。全身给药ANG II结合高盐饮食可诱发高血压，这可能与SNA升高有关。然而，RVLM血管运动神经元在ANG ii型盐性高血压中的功能作用尚未确定。在此，我们验证了ANG ii型盐性高血压大鼠RVLM血管舒缩神经元在静息放电中有夸大的假设。高血压（HT）组大鼠进食高盐（2% NaCl）饮食，并注射ANG II (150 ng·kg−1·min−1sc)，持续14天。正常血压（NT）组大鼠进食正常盐（0.4% NaCl）饮食，并注入生理盐水。有意识大鼠的遥测记录显示，与NT大鼠相比，HT组的平均动脉压（MAP）显著升高（P< 0.001）。在麻醉（氨基甲酸乙酯/氯氯蔗糖）下，与NT大鼠相比，HT大鼠的MAP仍然升高（P< 0.01）。HT （n= 28）和NT （n= 22）大鼠的细胞外单单位记录显示，两组（HT， 23个细胞；NT， 34个细胞）的压敏RVLM神经元具有相似的心律和静息放电。然而，相比NT（28个细胞，29±3 mmHg）大鼠，HT（17个细胞，44±5 mmHg）大鼠需要更多的MAP来抑制神经元放电（P< 0.01）。动脉压力感受器卸荷时的最大放电率各组相似。我们得出结论，交感兴奋性RVLM神经元的静息放电增高对于维持神经源性angii盐性高血压并不是必需的。
Neurons of the rostral ventrolateral medulla (RVLM) are critical for generating and regulating sympathetic nerve activity (SNA). Systemic administration of ANG II combined with a high-salt diet induces hypertension that is postulated to involve elevated SNA. However, a functional role for RVLM vasomotor neurons in ANG II-salt hypertension has not been established. Here we tested the hypothesis that RVLM vasomotor neurons have exaggerated resting discharge in rats with ANG II-salt hypertension. Rats in the hypertensive (HT) group consumed a high-salt (2% NaCl) diet and received an infusion of ANG II (150 ng·kg−1·min−1sc) for 14 days. Rats in the normotensive (NT) group consumed a normal salt (0.4% NaCl) diet and were infused with normal saline. Telemetric recordings in conscious rats revealed that mean arterial pressure (MAP) was significantly increased in HT compared with NT rats (P< 0.001). Under anesthesia (urethane/chloralose), MAP remained elevated in HT compared with NT rats (P< 0.01). Extracellular single unit recordings in HT (n= 28) and NT (n= 22) rats revealed that barosensitive RVLM neurons in both groups (HT, 23 cells; NT, 34 cells) had similar cardiac rhythmicity and resting discharge. However, a greater (P< 0.01) increase of MAP was needed to silence discharge of neurons in HT (17 cells, 44 ± 5 mmHg) than in NT (28 cells, 29 ± 3 mmHg) rats. Maximum firing rates during arterial baroreceptor unloading were similar across groups. We conclude that heightened resting discharge of sympathoexcitatory RVLM neurons is not required for maintenance of neurogenic ANG II-salt hypertension.
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