Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.

Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.
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自发性高血压大鼠突触前α-和β-肾上腺素受体刺激和去甲肾上腺素释放。

DOI:
10.1161/01.hyp.5.2.198
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发表时间:
1983
期刊:
影响因子:
8.3
通讯作者:
M. Lokhandwala
M. Lokhandwala
中科院分区:
医学1区
文献类型:
--
作者:
R. Ekas;M. Steenberg;M. Woods;M. Lokhandwala

文献摘要

被引文献

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本研究在正常血压的Wistar-Kyoto(WKY)和自发性高血压大鼠(SHR)离体灌流肾脏中,测定了交感神经刺激时去甲肾上腺素的释放,并分别评价了α-肾上腺素受体激动剂和β-肾上腺素受体激动剂的突触前抑制和易化作用。动脉周围神经刺激(0.25至32 Hz)引起显着更大的释放去甲肾上腺素,这是衡量为总氚溢出,在SHR。血管收缩反应动脉周围神经刺激以及去甲肾上腺素,血管紧张素II,氯化钡也显着更大的SHR。在2 Hz的动脉周围神经刺激过程中,测定了α 2-肾上腺素受体激动剂曲马唑和α 32-肾上腺素受体激动剂沙丁胺醇对去甲肾上腺素释放的突触前作用。曲马唑啉(2 × 10~(-9)~ 2 × 10 ~(-7)M)对SHR的去甲肾上腺素释放有浓度依赖性抑制作用,但对WKY无抑制作用。虽然最高浓度的曲马唑啉(2 × 10 - 7 M)在WKY中发挥抑制作用,但这种作用的程度低于在SHR中观察到的作用。沙丁胺醇(10~(10)~ 10~(16)M)可增加动脉周围神经刺激时去甲肾上腺素的释放,但β-肾上腺素受体激动剂的这种作用在WKY和SHR中相似。这些结果表明,去甲肾上腺素释放交感神经刺激时显着更大的SHR,这种现象可能有助于维持高血压。虽然WKY和SHR的突触前α-肾上腺素受体功能相似,但SHR的突触前α-肾上腺素受体是超敏感的。这种超敏感性可能是生理上的重要性,在削减已经更大的释放去甲肾上腺素在SHR。(高血压5:198-204,1983)
The present study was designed to measure norepinephrine release during sympathetic nerve stimulation and evaluate the presynaptic inhibitory and facilitatory actions of a-adrenoceptor and/3-adrenoceptor agonists respectively, in the isolated perfused kidney of normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Periarterial nerve stimulation (0.25 to 32 Hz) caused a significantly greater release of norepinephrine, which was measured as total tritium overflow, in the SHR. The vasoconstrictor responses to periarterial nerve stimulation as well as to norepinephrine, angiotensin II, and barium chloride were also significantly greater in the SHR. Presynaptic actions of tramazoltne, an a2-adrenoceptor agonist, and salbutamol, a/32-adrenoceptor agonist, on norepinephrine release were determined during periarterial nerve stimulation at 2 Hz. Tramazoline (2 x 10~ 9 to 2 x 10" 7 M) caused a concentration-dependent inhibition of stimulusinduced release of norepinephrine in SHR but not in WKY. While the highest concentration of tramazoline (2 x 10" 7 M) exerted an inhibitory action in the WKY, this effect was of lesser magnitude than that seen in SHR. Salbutamol (10~ 10 to 10~ 6 M) produced an increase in norepinephrine release during periarterial nerve stimulation; however, this action of the/3-adrenoceptor agonist was similar in both the WKYand SHR. These results demonstrate that norepinephrine release during sympathetic nerve stimulation is significantly greater in the SHR, and this phenomenon may contribute to the maintenance of hypertension. While presynaptic/3-adrenoceptor function is similar in both the WKY and SHR, presynaptic a-adrenoceptors are supersensitive in the SHR. This supersensitivity may be of physiological importance in curtailing an already greater release of norepinephrine present in the SHR.(Hypertension 5: 198-204, 1983)