The possibility that hypertension could be reproduced by renin was first explored by HESSEL (1) who in 1938 reported that daily intravenous injections of crude rabbit renin into rabbits lead to sustained hypertension which in one animal lasted 7 months after cessation of treatment. Hypertension developed in spite of tachyphylaxis and was accompanied, as in severe renal hypertension, by proteinuria and urinary casts and red blood cells. However, these results could not be confirmed by STREHLER and SUTER (2), who attributed the sustained hypertension to chronic nephritis, either as a naturally-occuring disease or as the result of infection caused by bacterial contamination of kidney extracts. In 1939 HILL and PICKERING (3) observed that intravenous infusion into rabbits of small doses of rabbit renin caused a rise in pressure which was maintained only for the duration of the infusion. With larger doses there was a more pronounced rise, which was, however, followed by a return toward normal levels in spite of the continued infusion. Even when the period of infusion was extended up to 18 days, hypertension did not become self-sustained and no hypertensive vascular lesions were observed (4, 5). Similar observations were made by TAGGART and DRURY (6) who further noted that the high blood pressure level of hypertensive animals could not be equated with renin infusion, that the response to renin of hypertensive animals differed quantitatively and qualitatively from that in normal animals and finally that renin tachyphylaxis did not alleviate hypertension. On this basis they concluded that established renal hypertension was not due to renin. Subcutaneous like intravenous administration of renin to uninephrectomized rats caused massive diuresis but only a slight rise in pressure and no vascular lesions (7). To these observations one should add the unsuccessful attempts to transfer hypertension by massive blood transfusion from hypertensive into normal or bilaterally nephrectomized animals (8, 9). The investigations of WINTERNITZ et al. (10) and of LEITER and EICHELBERGHER (11) were concerned with acute hypertension as it occurs after bilateral ligation or severe clamping of renal arteries. Intravenous injections of kidney extracts into bilaterally nephrectomized animals or animals with reduced excretory function caused a prolonged rise in pressure and vascular lesions reminiscent of malignant hypertension. Since these results could not be obtained in normal animals, it was evident that renal insufficiency had some sensitizing effect. Subcutaneous like intravenous administration of renin to bilaterally nephrectomized dogs given 1% saline to drink also caused a sustained rise in pressure accompanied by hemorrhages and vascular necrosis (12).
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