抄録
It is clear that defective renal sodium handling plays an important role in the development of hypertension and that this abnormality could be caused by heterogeneous hereditary factors in the kidney. It is likely that sodium pump inhibitors with or without whole-body autoregulation gradually produce a rise in blood pressure in response to retained body sodium. Accumulated evidence has suggested that several sodium pump inhibitors similar to cardiotonic steroids are present in the human body. Ouabainlike compound (OLC) has been found to be increased with high sodium intake and hypervolemia, and in essential hypertension, mineralocorticoid hypertension, and pregnancy-induced hypertension. Further, blocking the action of OLC with digibind or a novel anti-ouabain agent has been observed to lower blood pressure in several models of experimental and clinical hypertension. The blockade of OLC action may become the basis of novel rational antihypertensive agents and may help to solve the problems still present in the management of hypertensive patients. (Hypertens Res 2000; 23 Suppl: S7-S13)
