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自发性高血压大鼠肾上腺交感神经活动对神经节阻断、精神应激和神经低血糖的高反应性。

Hyper-responsiveness of adrenal sympathetic nerve activity in spontaneously hypertensive rats to ganglionic blockade, mental stress and neuronglucopenia.

作者信息

Zhang W, Thorén P

机构信息

Department of Physiology and Pharmacology, Karolinska Institute, 171 77 Stockholm, Sweden.

出版信息

Pflugers Arch. 1998 Dec;437(1):56-60. doi: 10.1007/s004240050746.

DOI:10.1007/s004240050746
PMID:9817786
Abstract

Previous investigations indicate that the spontaneously hypertensive rat (SHR) has elevated sympathetic tone at rest. The present study aimed to determine whether SHR has exaggerated sympatho-adrenal activation in response to various sympathetic stimuli. The mean blood pressure (MBP), heart rate (HR) and preganglionic adrenal sympathetic nerve activity (SNA) were recorded from conscious, unrestrained SHR and from its normotensive control, the Wistar-Kyoto rat (WKY) (n=7, respectively).Ganglionic blockade (trimethaphan, 5 mg/kg) reduced MBP identically in both groups of rats. It did not change HR in SHR, but increased HR significantly in WKY (P<0.05). The adrenal SNA increased in both groups, but the magnitude of the increase was more than threefold greater in SHR (P<0.05). Mental stress caused by air-jet induced significantly greater tachycardia (threefold) and sympatho-adrenal activation (tenfold) in SHR than in WKY rats. In SHR the inhibition of glycolysis (2-deoxy-d-glucose, 500 mg/kg) also produced a profound activation of adrenal SNA (sevenfold) and the increased adrenal SNA was not paralleled by an increased HR. We conclude that a variety of sympathetic stimuli, including ganglionic blockade, mental stress and neuronglucopenia, cause exaggerated activation of preganglionic adrenal SNA in SHR compared with WKY, indicating that adrenal SNA in SHR is hyper-responsive.

摘要

先前的研究表明,自发性高血压大鼠(SHR)静息时交感神经张力升高。本研究旨在确定SHR对各种交感神经刺激的交感 - 肾上腺激活是否过度。记录清醒、不受约束的SHR及其血压正常的对照Wistar - Kyoto大鼠(WKY)(每组n = 7)的平均血压(MBP)、心率(HR)和肾上腺节前交感神经活动(SNA)。神经节阻断(阿方那特,5 mg/kg)使两组大鼠的MBP同等程度降低。它对SHR的HR无影响,但使WKY的HR显著增加(P<0.05)。两组的肾上腺SNA均增加,但SHR的增加幅度是WKY的三倍多(P<0.05)。喷气引起的精神应激在SHR中引起的心动过速(三倍)和交感 - 肾上腺激活(十倍)明显大于WKY大鼠。在SHR中,糖酵解抑制(2 - 脱氧 - d - 葡萄糖,500 mg/kg)也引起肾上腺SNA的显著激活(七倍),且肾上腺SNA增加并未伴随HR增加。我们得出结论,与WKY相比,包括神经节阻断、精神应激和神经元低血糖在内的多种交感神经刺激导致SHR中肾上腺节前SNA的激活过度,表明SHR中的肾上腺SNA反应过度。

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