Mitsuyasu Aida

Assay of Renin in Peripheral Blood

Long time has elapsed since the discovery of renin-angiotensin system as a possible cause of renal hypertension. But the role of this system in. the pathogenesis of renal or essential hypertension has been entirely unknown. Skeggs et al.1) found increased angiotensin in arterial blood not only in renal and malignant hypertension but also in benign essential hypertension, and concluded that this increase in circulating angiotensin is the principal cause of these hypertensions. Dexter et al.2) and Scornik et al.3) reported that release of renin from the kidney increases only in the initial stage of experimental renal hyperten sion, but it decreases to normal level in the chronic phase in spite of sustained hypertension. Peart4) discussed that the renin-angiotensin system has no relationship to the causation or maintenance of all kinds of hypertension , either renal or malignant. What is the reason of this discrepancy? It has been stressed in answer to this question that there was no reliable method for the estimation of renin or angiotensin in low concentrations as expected in renal or peripheral blood , and that development of such a method is urgently demanded to elucidate this conflic ting problem. New methods were introduced in 1961 by Scornik et al .3) and Boucher et al.5) for the determination of angiotensin in arterial blood , but they are not easily applicable because of the complexity in procedures and the need of large amounts of blood. Recently Helmer6) proposed a simple technique for the detection of renin in renal or peripheral blood. It consisted of dialysis of plasma to remove active substances of low molecular weight and direct assay of the dialyzed plasma on an isolated rabbit aortic strip. He further described that heat-stable and