Fujito K, Yokomatsu M, Numahata H, Ishiguro N, Koide H
Department of Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Life Sci. 1992;51(26):2079-87. doi: 10.1016/0024-3205(92)90159-m.
The acute effects of angiotensin-converting enzyme inhibitor, captopril, on sodium ion transport systems were investigated in essential hypertensive and normotensive subjects. The passive sodium efflux through the erythrocyte membrane was significantly higher and erythrocyte sodium-potassium cotransport was lower in patients with essential hypertension when compared with normal subjects. However, sodium-potassium pump activity and sodium-lithium countertransport did not differ significantly between the hypertensive patients and the normal subjects. Immediately after captopril administration, erythrocyte passive sodium efflux and sodium-potassium cotransport returned to normal levels in the hypertensive subjects. Although the plasma renin activity and plasma aldosterone concentration were altered by captopril, they did not correlate with changes in any sodium transport system. These results suggest that the changes in sodium transport systems which occur immediately after captopril administration may contribute, at least in part, to its antihypertensive action.
在原发性高血压患者和血压正常者中，研究了血管紧张素转换酶抑制剂卡托普利对钠离子转运系统的急性作用。与正常受试者相比，原发性高血压患者红细胞膜的被动钠外流显著更高，而红细胞钠钾协同转运更低。然而，高血压患者与正常受试者之间的钠钾泵活性和钠锂逆向转运没有显著差异。卡托普利给药后，高血压受试者的红细胞被动钠外流和钠钾协同转运立即恢复到正常水平。虽然卡托普利改变了血浆肾素活性和血浆醛固酮浓度，但它们与任何钠转运系统的变化均无相关性。这些结果表明，卡托普利给药后立即出现的钠转运系统变化可能至少部分促成了其降压作用。
