Myers J H, Lamb F S, Webb R C
J Hypertens. 1987 Apr;5(2):161-71. doi: 10.1097/00004872-198704000-00006.
This study characterizes contractions to ouabain and potassium-free solution in isolated vascular segments from two-kidney, one clip (2-K, 1C) hypertensive rats. Aorta, mesenteric artery, and vena cava from hypertensive rats were more sensitive (lower threshold) to ouabain than those from normotensive rats. Contractions of hypertensive vascular segments to potassium-free solution and to ouabain (10(-3) mol/l) were faster than those in normotensive vessels. Monensin potentiated contractions to ouabain and increased the rate of force development to potassium-free solution to a greater extent in normotensive aortae than in hypertensive aortae. Amiloride, low sodium solution, verapamil and calcium-free solution depressed contractions to ouabain and potassium-free solution in both hypertensive and normotensive aortae. These observations demonstrate augmented responsiveness to ouabain and potassium-free solution in hypertensive blood vessels. Interventions which influence transmembrane sodium and calcium movements altered contractions to ouabain and potassium-free solution. The results are consistent with the hypothesis that vascular cells of hypertensive rats have enhanced sodium pump activity.
本研究对两肾一夹（2-K，1C）高血压大鼠离体血管段对哇巴因和无钾溶液的收缩反应进行了表征。高血压大鼠的主动脉、肠系膜动脉和腔静脉对哇巴因的敏感性（阈值更低）高于正常血压大鼠。高血压血管段对无钾溶液和哇巴因（10⁻³mol/L）的收缩反应比正常血压血管更快。莫能菌素增强了对哇巴因的收缩反应，并且在正常血压主动脉中比在高血压主动脉中更大程度地提高了对无钾溶液的力量发展速率。氨氯地平、低钠溶液、维拉帕米和无钙溶液在高血压和正常血压主动脉中均抑制了对哇巴因和无钾溶液的收缩反应。这些观察结果表明高血压血管对哇巴因和无钾溶液的反应性增强。影响跨膜钠和钙运动的干预措施改变了对哇巴因和无钾溶液的收缩反应。结果与高血压大鼠血管细胞钠泵活性增强的假说一致。
