The etiology of clinical hypertension is still unknown. Very little has been added to the knowledge of the subject since Janeway's masterly reviews in 19041 and 1913.2 The center of interest has shifted from the rôle of the kidneys to the influence of hyperirritable vasomotor centers, inadequate depressor reflexes (carotid sinuses and aorta), excessive or unbalanced action of chemical pressor substances in the circulating blood, physicochemical changes in the arteriolar media (premature "aging"?)—in short, all the possible physiologic mechanisms involved in the regulation of blood pressure. To complete the circle, the kidneys have again been placed in the foreground by the recent ingenious experiments of Goldblatt and his associates.3 Their results are particularly significant because for the first time hypertension has been produced in the experimental animal by obstruction of the renal arteries without the necessary association of renal insufficiency.
The difficulty of analyzing the actual nature