Sodium responsiveness of central alpha 2-adrenergic receptors in spontaneously hypertensive rats.

Sodium responsiveness of central alpha 2-adrenergic receptors in spontaneously hypertensive rats.
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自发性高血压大鼠中枢α2-肾上腺素能受体的钠反应性。

DOI:
10.1161/01.hyp.11.4.326
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发表时间:
1988
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
DiBona,GF
DiBona,GF
中科院分区:
--
文献类型:
--
作者:
Koepke,JP;Jones,S;DiBona,GF

文献摘要

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比较了有意识自发性高血压大鼠(SHR)和正常Wistar-Kyoto大鼠(WKY)在正常或高钠摄入(3-4周1% NaCl饮用)时中枢神经系统α 2-肾上腺素能受体对肾功能神经控制的反应性。通过比较各组间累积注射胍那苯(5、25和125微克)对平均动脉压、肾交感神经活动和尿钠排泄影响的剂量-反应曲线,确定中枢α 2-肾上腺素能受体的反应性。瓜纳苯对正常或高钠摄入的SHR和正常或高钠摄入的WKY的平均动脉压的改变类似。高钠摄取量使鸟那苯-肾交感神经活动和鸟那苯-尿钠排泄剂量-反应曲线在SHR组左移,在WKY组右移。SHR和WKY对正常钠摄入量的剂量-反应曲线相似。在正常或高钠摄入的SHR和WKY患者中,手术肾去神经或使用α - 2-肾上腺素受体拮抗剂(山竹碱,30微克i.c.v)预处理会减弱胍那苯对肾交感神经活动的抑制能力或增加尿钠排泄的能力。我们的结论是,在有意识的SHR中,高钠摄入增加了中枢神经系统α - 2-肾上腺素能受体对肾功能神经控制的反应性,而在有意识的正常血压的WKY中则没有。
The responsiveness of central nervous system alpha 2-adrenergic receptors in the neural control of renal function was compared in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) on normal or high sodium intake (3-4 weeks of 1% NaCl for drinking). The responsiveness of central alpha 2-adrenergic receptors was determined by comparing among groups the dose-response curves for the effects of cumulative intracerebroventricular injections of guanabenz (5, 25, and 125 micrograms) on changes in mean arterial pressure, renal sympathetic nerve activity, and urinary sodium excretion. Guanabenz altered mean arterial pressure similarly in SHR on normal or high sodium intake and in WKY on normal or high sodium intake. High sodium intake shifted the guanabenz-renal sympathetic nerve activity and guanabenz-urinary sodium excretion dose-response curves to the left in SHR and to the right in WKY. The dose-response curves between SHR and WKY on normal sodium intake were similar. Surgical renal denervation or pretreatment with an alpha 2-adrenergic receptor antagonist (rauwolscine, 30 micrograms i.c.v.) attenuated the ability of guanabenz to inhibit renal sympathetic nerve activity or increase urinary sodium excretion in SHR and WKY on either normal or high sodium intake. We conclude that the responsiveness of central nervous system alpha 2-adrenergic receptors regarding the neural control of renal function is increased by high sodium intake in conscious SHR, but not in conscious normotensive WKY.