The diverse effects of noradrenaline and other stimulants on 86Rb and 42K efflux in rabbit and guinea‐pig arterial muscle.
The diverse effects of noradrenaline and other stimulants on 86Rb and 42K efflux in rabbit and guinea‐pig arterial muscle.
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去甲肾上腺素和其他兴奋剂对兔和豚鼠动脉肌肉 86Rb 和 42K 流出的不同影响。
DOI：
10.1113/jphysiol.1984.sp015405
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
L. Clapp
中科院分区：
文献类型：
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作者：
T. Bolton;L. Clapp
本文研究了去甲肾上腺素和提高外部钾（[K+]o）对86 Rb或42 K流出和张力的影响。在所研究的动脉中，去甲肾上腺素（10（-5）-10（-4）M）诱发的最大86 Rb流出量存在10倍的变化，即使产生的张力相当。动脉收缩伴随86 Rb流出量的大幅增加，例如兔耳动脉和主动脉、豚鼠和兔肺动脉，或伴随小幅增加，例如兔和豚鼠肠系膜动脉、兔肱动脉和豚鼠腹主动脉。升高[K+]o对86 Rb和42 K外排也有不同的影响：去甲肾上腺素外排略有增加的动脉也对升高的[K+]o外排略有增加。在研究的动脉中，由升高的[K+]o引起的最大外排平均比由去甲肾上腺素引起的最大外排大三倍。外排反应的异质性无法通过去甲肾上腺素或升高的[K+]o对膜电位的影响的定量差异或α受体的差异来解释。在去甲肾上腺素诱发的86 Rb流出量较小的动脉中，组胺、5-羟色胺、加压素和血管紧张素也几乎没有影响。相反，去甲肾上腺素产生大量增加86 Rb流出的其他兴奋剂具有可比的效果。去除细胞外钙离子仅略微降低了兔主动脉中66 mM-外部K+诱发的86 Rb流出的增量，即使在这些条件下收缩几乎消失。在无钙条件下，10（-5）M去甲肾上腺素的情况下，40%的收缩仍然存在，其对外排的影响显著增加（P <0.05）。使用42 K获得了基本相似的结果。四乙基铵（10 - 20 mM）可显著降低[K+]o升高诱发的86 Rb外排（P <0.001），而仅轻微影响家兔主动脉中去甲肾上腺素诱发的外排。从血管肌肉的这些外排实验中得出结论，钾可以通过去极化和去甲肾上腺素激活α受体而逃逸的通道来自不同的人群，并且它们的性质在动脉之间存在差异。我们一直无法检测到任何实质性的钙激活成分在42 K或86 Rb流出反应提高[K+]o或去甲肾上腺素。
The effects of noradrenaline and of raised external potassium ([K+]o) on the efflux of 86Rb or 42K and on tension were studied in preparations taken from eight different arteries under various conditions. There was a 10‐fold variation in the maximum 86Rb efflux evoked by noradrenaline (10(‐5)‐10(‐4) M) in the arteries studied, even though tension generated was comparable. Arterial contractions were either accompanied by large increases in 86Rb efflux, e.g. rabbit ear artery and aorta, guinea‐pig and rabbit pulmonary artery, or by small increases, e.g. rabbit and guinea‐pig mesenteric artery, rabbit brachial artery and guinea‐pig abdominal aorta. Raising [K+]o also had a diverse effect on 86Rb and 42K efflux: arteries giving small increases in efflux to noradrenaline also gave small increases in efflux to raised [K+]o. The maximum efflux evoked by raised [K+]o was on average three times greater than the maximum efflux evoked by noradrenaline in the arteries studied. The heterogeneity of the efflux response could not be explained by the quantitative heterogeneity of the efflux response could not be explained by the quantitative differences in the effects of noradrenaline or of raised [K+]o on membrane potential or, in the case of noradrenaline, by differences in the alpha‐receptors. In arteries in which the noradrenaline‐evoked 86Rb efflux was small, histamine, 5‐hydroxytryptamine, vasopressin and angiotensin also had little effect. Conversely, where noradrenaline produced a large increase in 86Rb efflux those other stimulants had comparable effects. Removal of extracellular calcium only slightly reduced the increment in 86Rb efflux evoked by 66 mM‐external K+ in the rabbit aorta even though contractions were virtually abolished under these conditions. In the case of 10(‐5) M‐noradrenaline, 40% of the contraction remained and its effect on efflux was significantly increased (P less than 0.05) in calcium‐free conditions. Essentially similar results were obtained using 42K. Tetraethylammonium (10‐20 mM) produced a significant and substantial reduction (P less than 0.001) in the 86Rb efflux evoked by raised [K+]o while only slightly affecting the noradrenaline‐evoked efflux in the rabbit aorta. It was concluded from these efflux experiments on vascular muscle that the channels through which potassium can escape, opened by depolarization and by activation of alpha‐receptors with noradrenaline, are from different populations, and that their properties vary from one artery to another. We have been unable to detect any substantial calcium‐activated component in 42K or 86Rb efflux responses to raised [K+]o or to noradrenaline.