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血管紧张素对大鼠中枢组织去甲肾上腺素能神经传递的促进作用:钠限制的影响

Angiotensin facilitation of noradrenergic neurotransmission in central tissues of the rat: effects of sodium restriction.

作者信息

Meldrum M J, Xue C S, Badino L, Westfall T C

出版信息

J Cardiovasc Pharmacol. 1984 Nov-Dec;6(6):989-95.

PMID:6084790
Abstract

This study investigated the ability of angiotensin II (Ang II) to facilitate the stimulation-induced release of [3H]norepinephrine [( 3H]NE) from two cardiovascular regulatory areas in normal and sodium-restricted rats. Ang II (10(-7) M) facilitated the field-stimulation-induced release of [3H]NE from the A2 area of the nucleus tractus solitarius but not from the anterior hypothalamus of Sprague-Dawley and Wistar rats. Placement of rats on a sodium-restricted diet abolished the facilitation of [3H]NE release due to Ang II. Captopril given during sodium restriction partially restored the facilitory effects of Ang II. In an effort to determine the interaction of Ang II and sodium reduction, the effects of chronic Ang II were studied. Seven-day intravenous Ang II infusions blocked the facilitory effect of Ang II on [3H]NE release in a manner similar to that seen with sodium restriction. These results suggest that low sodium diets may alter the facilitation of [3H]NE release by Ang II by interactions with the renin-angiotensin system.

摘要

本研究调查了血管紧张素II(Ang II)促进正常和限钠大鼠两个心血管调节区域中刺激诱导的[3H]去甲肾上腺素([3H]NE)释放的能力。Ang II(10^(-7) M)促进了孤束核A2区域的场刺激诱导的[3H]NE释放,但未促进Sprague-Dawley和Wistar大鼠下丘脑前部的[3H]NE释放。将大鼠置于限钠饮食中可消除Ang II对[3H]NE释放的促进作用。限钠期间给予卡托普利可部分恢复Ang II的促进作用。为了确定Ang II与钠减少之间的相互作用,研究了慢性Ang II的作用。连续7天静脉输注Ang II以类似于限钠所见的方式阻断了Ang II对[3H]NE释放的促进作用。这些结果表明,低钠饮食可能通过与肾素-血管紧张素系统的相互作用改变Ang II对[3H]NE释放的促进作用。

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