Ito K
J Cardiovasc Pharmacol. 1982 Nov-Dec;4(6):889-94. doi: 10.1097/00005344-198211000-00003.
We have previously found that long-term blockade of angiotensin II (AII) formation by captopril suppresses the "leakiness" of vascular smooth muscle membrane from spontaneously hypertensive rats. The present study was undertaken to examine whether a subpressor concentration of AII alters the membrane permeability and the tension of vascular smooth muscle of rats. The isometric tensions of rat aortic strips were recorded and the cellular Na contents in the muscles were measured by the "cold Li-exchange method." Lowering external K+ concentration to 0 or 0.5 mM produced slowly developing contractions in the muscles. These contractions were significantly enhanced by 4 h of pretreatment with 3 X 10(-10) M AII, whereas there were no contractions in normal Tyrode solution. Increase in cellular Na during incubation in K+-free solution was greater in AII-pretreated muscles and the cellular Na in these muscles leaked out more rapidly into cold Li solution than it did in untreated muscles. These findings suggest that the subpressor concentration of AII increases the passive permeability of vascular smooth muscles to Na and, if the Na pump activity is partially impaired, elevates the vascular tone.
我们之前发现，卡托普利对血管紧张素II（AII）生成的长期阻断可抑制自发性高血压大鼠血管平滑肌膜的“渗漏性”。本研究旨在探讨亚升压浓度的AII是否会改变大鼠血管平滑肌的膜通透性和张力。记录大鼠主动脉条的等长张力，并用“冷锂交换法”测量肌肉中的细胞内钠含量。将细胞外钾离子浓度降至0或0.5 mM会使肌肉产生缓慢发展的收缩。用3×10⁻¹⁰ M AII预处理4小时可显著增强这些收缩，而在正常台氏液中则无收缩。在无钾溶液中孵育期间，AII预处理肌肉中的细胞内钠增加更多，且这些肌肉中的细胞内钠比未处理肌肉更快地泄漏到冷锂溶液中。这些发现表明，亚升压浓度的AII增加了血管平滑肌对钠的被动通透性，并且如果钠泵活性部分受损，则会升高血管张力。
