高血圧症と副腎皮質機能 : 第2篇実験高血圧症における副腎皮質機能

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It has been shown by Kumar and his associates that infusion of aldosterone (0.5 g/48 hr. or 1.O g/24hr.) elevates blood pressure in rats. By Gornall (1960), similar increases of blood pressure in responses to aldosterone (0.4〜0.5g/1OO g body weight) were reported in the same animal. It was opposed, however, by Gaint and Gross, who failed to induce experimental hypertension in rats in spite of long-term administration of aldosterone. At that period, numerous attempts were made to elucidate the mechanisms responsible for this experimental hypertension. However, thus far, direct evidence concerning the role of aldosterone in controlling blood pressure remained obscure. But a few groups, such as Gross and his collaborators, led to the same conclusion that, with the very small dosage of aldosterone, there was no increase in mean arterial pressure, although further progressive rise could be maintained by administration of a large amount of aldosterone (0.2mg/day). Besides, it was demonstrated that the hypertensogenic action of aldosterone in large doses was not so remarkable as that induced by infusion of deoxycorticosterone. On the other hand, persistent hypertension has been produced in animals by constricting the main renal arteries. This experimental hypertension, produced by Goldblatt (1934), reduces the blood flow to the functioning components of the kidneys.
社団法人日本泌尿器科学会の論文