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在去氧皮质酮盐性高血压中口服β受体阻滞剂对血管肾上腺素能神经元去甲肾上腺素释放的抑制作用

Inhibition of norepinephrine release from vascular adrenergic neurons by oral administration of beta-blocker in DOCA-salt hypertension.

作者信息

Tsuda K, Masuyama Y

机构信息

Department of Medicine, Wakayama Medical College, Japan.

出版信息

Am J Hypertens. 1991 Jan;4(1 Pt 1):68-71. doi: 10.1093/ajh/4.1.68.

Abstract

The ability of a beta-blocker to inhibit vascular sympathetic nerve activity associated with hypertension was studied in DOCA-salt hypertension in rats. A seven week treatment of DOCA and salt resulted in a significant increase in the systolic blood pressure of the uninephrectomized rats. The administration of propranolol (40 mg/L and 80 mg/L in drinking water) had little effect on the development of hypertension. After a three week administration of propranolol, perfused mesenteric vasculatures were prepared in vitro, and endogenous norepinephrine release as well as vascular responsiveness were examined. Endogenous norepinephrine and pressor responses during periarterial nerve stimulation were greater in the untreated DOCA-salt hypertensive rats than in the normotensive rats. In the DOCA-salt hypertensive rats treated with propranolol, the stimulation-evoked norepinephrine release and pressor responses were significantly attenuated, at both doses, compared with the untreated DOCA-salt hypertensive rats. These results demonstrate that propranolol inhibited the vascular sympathetic nerve activity in DOCA-salt hypertensive rats. This occurrence suggests a possible role of presynaptic beta-adrenoceptors in the regulation of sympathetic tone in DOCA-salt hypertension.

摘要

在去氧皮质酮盐诱导的大鼠高血压模型中,研究了β受体阻滞剂抑制与高血压相关的血管交感神经活动的能力。给予去氧皮质酮和盐七周后,单侧肾切除大鼠的收缩压显著升高。给予普萘洛尔(饮用水中浓度为40mg/L和80mg/L)对高血压的发展影响不大。给予普萘洛尔三周后,制备离体灌注肠系膜血管,检测内源性去甲肾上腺素释放以及血管反应性。未治疗的去氧皮质酮盐高血压大鼠在动脉周围神经刺激期间的内源性去甲肾上腺素和升压反应比正常血压大鼠更大。与未治疗的去氧皮质酮盐高血压大鼠相比,在接受普萘洛尔治疗的去氧皮质酮盐高血压大鼠中,两种剂量下刺激诱发的去甲肾上腺素释放和升压反应均显著减弱。这些结果表明,普萘洛尔抑制了去氧皮质酮盐高血压大鼠的血管交感神经活动。这一现象提示突触前β肾上腺素受体在去氧皮质酮盐高血压中交感神经张力调节中可能发挥作用。

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