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[肾上腺素能β受体阻滞剂的降压作用及其对自发性高血压大鼠整个交感神经输出的影响]

[Antihypertensive action of adrenergic beta-receptor blockers and its effect on the entire sympathetic outflow in spontaneously hypertensive rats].

作者信息

Ishimori T, Shiratsuchi K, Izumi A, Himori N

出版信息

Nihon Yakurigaku Zasshi. 1982 Dec;80(6):463-9.

PMID:6131020
Abstract

Three kinds of beta-adrenoceptor blocking agents were orally administered to spontaneously hypertensive rats (SH rats) from 5 to 13 weeks of age, and their effects on the development of hypertension and on peripheral sympathetic nervous system were investigated. In SH rats treated with the vehicle (2% Tween 80) for 8 weeks, systolic blood pressure increased from 132 +/- 1.3 to 179 +/- 2.7 mmHg (n = 10). Treatment with propranolol (2 X 50 mg/kg/day p.o., n = 8), pindolol (2 X 15 mg/kg/day p.o., n = 8) and D-32 (2 X 15 or 2 X 50 mg/kg/day p.o., n = 9) for 8 weeks slightly but definitely depressed the aforesaid development of hypertension, and their average reduction in systolic blood pressure was approximately 15 mmHg. In the pressor response to electrical stimulation of pre-ganglionic sympathetic nerves, there was not any difference between SH rats treated with vehicle and beta-adrenoceptor blocking agents (propranolol and D-32). P.o. administration of guanethidine or phentolamine, however, caused a slight hypotension and produced a significant reduction in the pressor response to electrical stimulation. SH rats treated with propranolol showed a leftward shift of the pressor response curve not to norepinephrine but to angiotensin II as compared with that obtained from vehicle treated SH rats. This phenomenon is probably due to the decreased renin release by the prolonged-treatment with drug. On the basis of these results, we could not obtain any clear evidence that the antihypertensive action exerted by beta-adrenoceptor blocking agents resulted from some interference with the function of the peripheral sympathetic nervous system.

摘要

对5至13周龄的自发性高血压大鼠(SH大鼠)口服三种β-肾上腺素能受体阻滞剂,研究它们对高血压发展及外周交感神经系统的影响。用赋形剂(2%吐温80)处理8周的SH大鼠,收缩压从132±1.3 mmHg升至179±2.7 mmHg(n = 10)。用普萘洛尔(2×50 mg/kg/天,口服,n = 8)、吲哚洛尔(2×15 mg/kg/天,口服,n = 8)和D - 32(2×15或2×50 mg/kg/天,口服,n = 9)处理8周,可轻微但确切地抑制上述高血压的发展,它们使收缩压平均降低约15 mmHg。在对节前交感神经电刺激的升压反应中,用赋形剂处理的SH大鼠与用β-肾上腺素能受体阻滞剂(普萘洛尔和D - 32)处理的SH大鼠之间没有差异。然而,口服胍乙啶或酚妥拉明会引起轻微低血压,并使对电刺激的升压反应显著降低。与用赋形剂处理的SH大鼠相比,用普萘洛尔处理的SH大鼠对去甲肾上腺素的升压反应曲线未发生左移,但对血管紧张素II的升压反应曲线发生了左移。这种现象可能是由于药物长期治疗导致肾素释放减少。基于这些结果,我们没有获得任何明确证据表明β-肾上腺素能受体阻滞剂的降压作用是由于对外周交感神经系统功能的某种干扰所致。

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