Riozzi A, Heagerty A M, Bing R F, Thurston H, Swales J D
Br Med J (Clin Res Ed). 1984 Oct 20;289(6451):1025-7. doi: 10.1136/bmj.289.6451.1025.
Leucocytes were isolated from venous blood of 11 normotensive volunteers with no family history of hypertension and the sodium efflux rate constants determined both alone and in the presence of increasing physiological concentrations of noradrenaline. There was a significant dose dependent reduction of total sodium efflux rate constant due to a reduction in ouabain sensitive sodium pump activity, glycoside insensitive efflux rate constants being unaffected. The magnitude of this effect was similar to the reduction in leucocyte sodium efflux rate constants observed in hypertensive patients (and their normotensive relatives). The noradrenaline induced depression of sodium pump activity was prevented by propranolol in a further seven experiments, suggesting that the effect was mediated by beta adrenoceptors. Catecholamines possibly functioning as circulating inhibitors of sodium transport may contribute to some of the disturbances in membrane electrolyte handling both in essential hypertension in man and in some experimental models of hypertension.
从11名无高血压家族史的血压正常志愿者的静脉血中分离出白细胞,分别测定其单独状态下以及在去甲肾上腺素生理浓度不断增加时的钠外流速率常数。由于哇巴因敏感的钠泵活性降低,总钠外流速率常数出现显著的剂量依赖性降低,而糖苷不敏感的外流速率常数未受影响。这种效应的程度与在高血压患者(及其血压正常的亲属)中观察到的白细胞钠外流速率常数降低相似。在另外七项实验中,普萘洛尔可防止去甲肾上腺素诱导的钠泵活性降低,这表明该效应是由β肾上腺素能受体介导的。儿茶胺可能作为循环中的钠转运抑制剂发挥作用,这可能导致人类原发性高血压以及一些高血压实验模型中膜电解质处理的某些紊乱。