Effects of Selective and Nonselective β-Agonists on Plasma Potassium and Norepinephrine
Effects of Selective and Nonselective β-Agonists on Plasma Potassium and Norepinephrine
复制标题
选择性和非选择性 β-激动剂对血浆钾和去甲肾上腺素的影响
DOI：
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发表时间：
1984
影响因子：
3
通讯作者：
M. Schalekamp
中科院分区：
文献类型：
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作者：
H. H. Vincent;F. Boomsma;A. J. Veld;F. H. Derkx;Wenting Gj;M. Schalekamp
在临界高血压受试者中，比较了 β 激动剂异丙肾上腺素（非选择性）、左旋普那特罗 β1 选择性）和沙丁胺醇（β2 选择性）分级输注对血浆钾和去甲肾上腺素的影响。所有三种激动剂的钾水平均下降，异丙肾上腺素和沙丁胺醇的去甲肾上腺素水平上升。这些对钾和去甲肾上腺素的影响密切相关，并且发生在与心血管反应相同的剂量范围内。血浆钾的下降可能是由于β受体的激活引起的，主要是骨骼肌上的β受体，随后刺激钠钾跨细胞膜的转运。血浆去甲肾上腺素的升高可能是由于交感神经末梢上的β受体激活所致。已知这些突触前受体的激活可增强神经刺激期间去甲肾上腺素的释放。对于心率和心肌收缩力的给定增加（通过心率校正的总机电收缩持续时间（主要是 β1 反应）测量），对钾和去甲肾上腺素的影响顺序为：沙丁胺醇 > 异丙肾上腺素 > 普那特罗。 β-阻断用普萘洛尔（非选择性）80 mg，每天四次，或阿替洛尔（β1-选择性），100 mg，每天一次，拮抗异丙肾上腺素的低钾作用以及去甲肾上腺素的升高，但当异丙肾上腺素输注剂量足够高以克服心率反应的阻断时，对去甲肾上腺素和钾的影响被消除是普萘洛尔而不是阿替洛尔。因此，所讨论的受体似乎属于β2亚型。众所周知，肾上腺素在压力条件下会以高浓度循环，通常被认为是这些受体的内源性激活剂。 β-受体阻滞剂可以预防低钾血症，并可以抑制交感神经活动，这可能有助于其所谓的心脏保护作用。这里和其他研究中提供的证据表明，β2 型受体参与应激引起的低钾血症和突触前促进去甲肾上腺素释放，值得进一步考虑 β 受体阻滞剂选择性的临床意义。
The effects of graded infusions of the β-agonists isoproterenol (nonselective), l-prenalterol β1-selective), and salbutamol (β2-selective) on plasma potassium and norepinephrine were compared in subjects with borderline hypertension. Potassium levels fell with all three agonists, and norepinephrine levels rose with isoproterenol and salbutamol. These effects on potassium and norepinephrine were closely correlated and occurred at the same dose ranges as the cardiovascular responses. The fall in plasma potassium was probably caused by activation of β-receptors, mainly on skeletal muscle, with subsequent stimulation of active sodium-potassium transport across the cellular membrane. The rise in plasma norepinephrine may have been due to activation of β-receptors on sympathetic nerve endings. Activation of these presynaptic receptors is known to enhance the release of norepinephrine during nerve stimulation. For a given increase in heart rate and cardiac contractility, as measured by the heart rate-corrected duration of total electromechanical systole, which are mainly β1-responses, the effects on potassium and norepinephrine were in the order: salbutamol > isoproterenol > prenalterol. β-Blockade with propranolol (nonselective), 80 mg four times a day, or atenolol (β1-selective), 100 mg once a day, antagonized the hypokalemic effect of isoproterenol as well as the rise in norepinephrine, but when isoproterenol was infused in doses high enough to overcome the blockade of the heart rate response, the effects on norepinephrine and potassium were abolished by propranolol and not by atenolol. Thus, the receptors in question appear to be of the β2-subtype. Epinephrine, which is known to circulate in high concentrations under stressful conditions, is generally considered to be the endogenous activator of these receptors. β-Blockers may prevent hypokalemia and may suppress sympathetic activity, which could contribute to their so-called cardioprotective action. The evidence presented here and in other studies that β2-type receptors are involved in stress-induced hypokalemia and in presynaptic facilitation of norepinephrine release warrants further consideration of the clinical significance of β-blocker selectivity.