高血圧症と副腎皮質機能

第1篇 副腎皮質機能より見た高血圧患者の検討

抄録

In 1898, Tigerstedt and Bergman detected a thermolabile, nondialyzable substance capable of increasing blood pressure in the extract of the rabbit kidney. Since then, the presence of this substance has been confirmed by a number of investigators. The name “renin” was given to this substance which integrated the humoral and neural elements of the renin-angiotensin system. However, its chemical structure is not clear even today. In 1934, Goldblatt and his associates succeeded in producing a persistent hypertension in dogs by constricting the main renal arteries. Their study was followed by others, in which the methods were modified to yield more reproducing results. In 1939, Page and Braun-Menendez independently discovered that renin itself had no activity to elevate blood pressure, but angiotensin possessed such an action. In 1953, Simpson & Reichstein isolated aldosterone as crystal. In 1955, Conn reported the presence of primary aldosteronism. Since then, attention has been paid to several features of aldosterone, such as enhancement of sodium transport, effection circulating blood volume and elevation of blood pressure. In 1960, Davis and his collaborators clarified that aldosterone-stimulating hormone (ASH), secreted from the kidney, might be identical with renin. Biron and his associates as well as Laragh and his collaborators discussed about the parallelism between the aggravation of hypertension and the increase of aldosterone secretion. After that, Marx confirmed from his experiments with unilaterally nephrectomized rats, that renin or angiotensin was related to the occurrence of hypertension. Cubbin obtained the same results. Observations on the adrenals in patients with hypertension secondary to renal or adrenal disorders suggested that these glands might play some role in the pathogenesis of hypertension. Therefore, it is considered that the responses to the reninangiotensin-aldosterone system might be occurred even in normotensive subjects. On the contrary, De Champlain could never find any increase in renin or angiotensin even in the case of renal hypertension. In short, it is a recent tendency to stress the role of renin as an aldosterone-stimulating factor rather than as a factor to participate in blood pressure elevation. Yet no definite conclusions have been drawn on the significance of the renin-angiotensin-aldosterone system in hypertension. The adrenal function has not completely been clarified morphologically by postmortem autopsy. Since adrenal biopsy is difficult on account of its locality, no sufficient investigation has been made on the adrenal function. To elucidate the function of the human adrenal cortex, histopathological as well as histochemical studies were carried out. In addition, vascular lesions of the kidneys and its relation to hypertension were discussed with the urinary aldosterone excretion.