Bolton T B, Clapp L H
J Physiol. 1984 Oct;355:43-63. doi: 10.1113/jphysiol.1984.sp015405.
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.
在不同条件下，对取自八条不同动脉的标本研究了去甲肾上腺素和细胞外钾浓度升高（[K⁺]ₒ）对⁸⁶Rb或⁴²K外流以及张力的影响。在所研究的动脉中，去甲肾上腺素（10⁻⁵ - 10⁻⁴M）诱发的最大⁸⁶Rb外流存在10倍的差异，尽管产生的张力相当。动脉收缩要么伴随着⁸⁶Rb外流大幅增加，例如兔耳动脉和主动脉、豚鼠和兔肺动脉，要么伴随着小幅增加，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⁸⁶Rb和⁴²K外流也有不同影响：对去甲肾上腺素外流增加较小的动脉，对升高的[K⁺]ₒ外流增加也较小。在所研究的动脉中，升高[K⁺]ₒ诱发的最大外流平均是去甲肾上腺素诱发最大外流的三倍。外流反应的异质性无法用去甲肾上腺素或升高的[K⁺]ₒ对膜电位影响的定量差异来解释，就去甲肾上腺素而言，也无法用α受体的差异来解释。在去甲肾上腺素诱发的⁸⁶Rb外流较小的动脉中，组胺、5 - 羟色胺、血管加压素和血管紧张素也几乎没有影响。相反，在去甲肾上腺素使⁸⁶Rb外流大幅增加的地方，其他那些刺激物有类似的作用。去除细胞外钙仅略微降低了兔主动脉中66 mM细胞外K⁺诱发的⁸⁶Rb外流增加，尽管在这些条件下收缩几乎完全被消除。对于10⁻⁵M去甲肾上腺素，40%的收缩仍然存在，并且在无钙条件下其对外流的影响显著增加（P < 0.05）。使用⁴²K获得了基本相似的结果。四乙铵（10 - 20 mM）使升高的[K⁺]ₒ诱发的⁸⁶Rb外流显著大幅降低（P < 0.001），而对兔主动脉中去甲肾上腺素诱发的外流仅略有影响。从这些对血管平滑肌的外流实验得出结论，钾外流所通过的通道，由去极化和去甲肾上腺素激活α受体而开放，来自不同群体，并且它们的特性因动脉而异。我们未能在对升高的[K⁺]ₒ或去甲肾上腺素的⁴²K或⁸⁶Rb外流反应中检测到任何大量的钙激活成分。
