血管紧张素II对大鼠子宫肌层离子通量的影响。

Effects of angiotensin II on ionic fluxes in rat myometrium.

Hamon G, Moura A M, Papadimitriou A, Worcel M

J Pharmacol. 1982 Apr-Jun;13(2):329-40.

Abstract

The action of angiotensin II (At II) on 24Na, 42K and 36 Cl fluxes was examined using longitudinal strips of rat myometrium as an experimental model. 2. In normally polarized muscles, At II 3.3 x 10(-6)M, a concentration 10 times higher than necessary to produce a maximal contraction of the muscle, increases 42K and 36 Cl efflux rates as well as 42K uptake. The action of At II on 42K and 36Cl effluxes is concentration-dependent. Under the same conditions 24Na efflux is not affected by At II, but a significant increase of 24Na uptake is obtained. In order to know whether the observed effects were membrane potential dependent, we reexamined the action of the peptide in preparations previously depolarized by a 101 mM K+ solution (K+ replacing Na+). In depolarized preparations, At II 3.3 x 10(-6)M still increases 24Na uptake, but the effects previously observed on 42K and 36Cl fluxes in normally polarized preparations are suppressed. It is concluded that At II produces a primary increase in the membrane permeability to Na+ and that the stimulation of 42K and 36Cl fluxes induced by At II in myometrial strips appears to be mainly potential dependent.

摘要

以大鼠子宫肌层的纵向条带作为实验模型，研究了血管紧张素II（At II）对24Na、42K和36Cl通量的作用。2. 在正常极化的肌肉中，At II（3.3×10⁻⁶M），该浓度比使肌肉产生最大收缩所需浓度高10倍，可增加42K和36Cl的外排速率以及42K的摄取。At II对42K和36Cl外排的作用呈浓度依赖性。在相同条件下，24Na外排不受At II影响，但24Na摄取显著增加。为了了解观察到的效应是否依赖于膜电位，我们重新研究了该肽在先前用101 mM K⁺溶液（K⁺替代Na⁺）去极化的制剂中的作用。在去极化的制剂中，At II（3.3×10⁻⁶M）仍可增加24Na摄取，但先前在正常极化制剂中观察到的对42K和36Cl通量的效应受到抑制。得出的结论是，At II使膜对Na⁺的通透性产生原发性增加，并且At II在子宫肌层条带中诱导的42K和36Cl通量的刺激似乎主要依赖于电位。