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血管紧张素II抑制自发性高血压大鼠下丘脑突触体中钾离子诱发的[3H]去甲肾上腺素释放。

Angiotensin II inhibits the K+-evoked release of [3H]norepinephrine from hypothalamic synaptosomes of the spontaneously hypertensive rat.

作者信息

Bottiglieri D F, Sumners C, Raizada M K

出版信息

Brain Res. 1987 Feb 10;403(1):167-71. doi: 10.1016/0006-8993(87)90139-9.

Abstract

The effect of angiotensin II on the basal and K+-evoked release of [3H]norepinephrine was examined in hypothalamic and brainstem synaptosomes from adult male normotensive (Wistar-Kyoto, WKY, and Sprague-Dawley, SD), and spontaneously hypertensive (SH) rats. Angiotensin II attenuated the [3H]norepinephrine release caused by maximal depolarizing concentrations of K+ (75 mM) in hypothalamic synaptosomes of the SH rat, but had no effect on basal [3H]norepinephrine release. Angiotensin II had no effect on either the basal or K+-evoked release of [3H]norepinephrine in brain synaptosomes prepared from either WKY or SD adult male rats. The results suggest a distinct role of angiotensin II in the modulation of catecholamine release in the SH rat.

摘要

研究了血管紧张素II对成年雄性正常血压大鼠(Wistar-Kyoto、WKY和Sprague-Dawley,SD)以及自发性高血压大鼠(SH)下丘脑和脑干突触体中[3H]去甲肾上腺素基础释放和钾离子诱发释放的影响。血管紧张素II减弱了SH大鼠下丘脑突触体中由最大去极化浓度钾离子(75 mM)引起的[3H]去甲肾上腺素释放,但对基础[3H]去甲肾上腺素释放没有影响。血管紧张素II对从WKY或SD成年雄性大鼠制备的脑突触体中[3H]去甲肾上腺素的基础释放或钾离子诱发释放均无影响。结果表明血管紧张素II在调节SH大鼠儿茶酚胺释放中具有独特作用。

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