Central vagal activation by alpha2-adrenergic stimulation is impaired in spontaneously hypertensive rats
Central vagal activation by alpha2-adrenergic stimulation is impaired in spontaneously hypertensive rats
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自发性高血压大鼠中α2-肾上腺素能刺激的中枢迷走神经激活受损
DOI：
10.1111/j.1748-1716.2012.02439.x
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发表时间：
2012
期刊：
影响因子：
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通讯作者：
et al
中科院分区：
文献类型：
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作者：
Kawada T;Akiyama T;Shimizu S;Kamiya A;Uemura K;et al
目的通过测量α2‐肾上腺素能刺激下左心室心肌间质乙酰胆碱（ACh）释放量，探讨自发性高血压大鼠（SHR）迷走神经控制异常。方法采用心脏微透析技术，观察美托咪定α2 -肾上腺素能刺激和迷走神经电刺激对正常血压Wistar-Kyoto大鼠（WKY）和SHR心肌间质乙酰胆碱（ACh）水平的影响。结果静脉滴注美托咪定（0.1 mg kg - 1）显著提高了WKY中乙酰胆碱含量（从2.4±0.6增加到4.2±1.3 nmol L−1，P< 0.05,n= 7），而SHR中无乙酰胆碱含量（从2.5±0.7增加到2.7±0.7 nmol L−1,n= 7）。相比之下，电迷走神经刺激增加了WKY（从1.0±0.4到2.9±0.9 nmol L−1，P< 0.001,n= 6）和SHR（从0.9±0.2到2.2±0.4 nmol L−1，P< 0.001,n= 6）的ACh水平。静脉注射美托咪定（0.1 mg kg−1）对WKY或SHR迷走神经刺激诱导的乙酰胆碱释放没有影响。结论美托咪定诱导的中枢迷走神经激活在SHR中受损，而外周迷走神经对乙酰胆碱释放的控制得以保留。除了交感神经控制异常外，中枢神经系统的迷走神经控制也可能在SHR中受损。
AimTo elucidate the abnormality of vagal control in spontaneously hypertensive rats (SHR) by measuring left ventricular myocardial interstitial acetylcholine (ACh) release in response to α2‐adrenergic stimulation as an index ofin vivovagal nerve activity.MethodsA cardiac microdialysis technique was applied to the rat left ventriclein vivo, and the effect of α2‐adrenergic stimulation by medetomidine or electrical vagal nerve stimulation on myocardial interstitial ACh levels was examined in normotensive Wistar–Kyoto rats (WKY) and SHR under anaesthetized conditions.ResultsIntravenous medetomidine (0.1 mg kg−1) significantly increased the ACh levels in WKY (from 2.4 ± 0.6 to 4.2 ± 1.3 nmol L−1,P< 0.05,n= 7) but not in SHR (from 2.5 ± 0.7 to 2.7 ± 0.7 nmol L−1,n= 7). In contrast, electrical vagal nerve stimulation increased the ACh levels in both WKY (from 1.0 ± 0.4 to 2.9 ± 0.9 nmol L−1,P< 0.001,n= 6) and SHR (from 0.9 ± 0.2 to 2.2 ± 0.4 nmol L−1,P< 0.001,n= 6). Intravenous administration of medetomidine (0.1 mg kg−1) did not affect the vagal nerve stimulation–induced ACh release in either WKY or SHR.ConclusionMedetomidine‐induced central vagal activation was impaired in SHR, whereas peripheral vagal control of ACh release was preserved. In addition to abnormal sympathetic control, vagal control by the central nervous system may be impaired in SHR.