The continuous secretion of renin by the chronically ischemic kidney was held to be unlikely in view of the experiments quoted by Dr. Kolff in which a rapid in situ transfer of an ischemic kidney to a normal dog did not raise the recipient's blood pressure. Measurable renin release was viewed rather as an acute intermittent response to a temporary reduction of renal circulation. Evidence from the classic experiment of Fasciolo, in which the transplanted chronic ischemic kidney caused hypertension in the recipient, was interpreted as showing the result of acute reduction in blood flow in the transplanted organ, rather than the chronic overproduction of renin. The depressor effect of antirenin injections in chronic renal hypertension might result from inhibition of the effect of renin on the hypothetical blood pressure regulating function of the normal kidney (Drs. Blaquier, Braun-Menéndez, Kolff).
The magnitude of pressor response to injected renin and angiotonin was discussed by Drs. Langford, Wakerlin and Helmer. The pulmonary hypertension produced by renin and angiotonin and the lack of an elevation in pulmonary blood pressure in experimental renal hypertensin was discussed by Drs. Langford, Wakerlin, Sancetta, Braun-Menéndez and Stamler.
Experiments disproving the importance of pulsatile flow as a stimulus to renin release were quoted by Dr. Kolff. An increase in the amount of the enzyme converting hypertensin I to its active form was considered as a possible mechanism for the production of hypertension by Drs. Leonard, Skeggs and Helmer.
The relative importance of pressure per se and of renal insufficiency in the production of the necrotizing vascular lesion of malignant hypertension was discussed by Drs. Robert and Goldblatt.
- © 1958 American Heart Association, Inc.