CONFERENCE on the role of the renal pressor system in maintenance of experimental renal hypertension.

Abstract

The hypothetical presence of increased circulating renin or hypertensin in chronic renal hypertension was debated; eventually it was agreed that methods were too insensitive for accurate assay. Pressor amounts of infused renin could not be detected by some methods of bioassay (Dr. Wakerlin). Hypertensinase activity in blood may destroy the end product before the assay can be performed (Dr. Blaquier). Perhaps rapid tissue removal from circulating blood may account for the inadequacy of the results (Dr. Skeggs). Previous experiments to detect these substances in circulating hypertensive blood have been indecisive (Dr. Braun-Menéndez) or only weakly positive (Drs. Goldblatt and Skeggs) and the clear-cut depressor effects of antirenin might act on a hypothetical nonpressor action of renin (Dr. Wakerlin). Dr. Helmer commented on the sustained pressor substance found in renal vein blood of hypertensive rats. Dr. Grollman believed chronic renal hypertension to be due to interference with an essential function of the kidney which in the normal animal prevents the blood pressure from rising. The failure of the blood pressure to rise when the kidneys from renal hypertensive dogs were perfused in situ by normotensive recipients was again discussed by Drs. Surtshin, Goldblatt and Grollman, and the possible fallacies involved in reasoning from such acute experiments were brought out. The nature of the stimulus to renin release was discussed again by Dr. Kolff. Non pulsatile flow was probably not a requirement (Dr. Kolff), nor was renal ischemia (Dr. Wakerlin), but some alteration in renal function seemed to be necessary (Dr. Goldblatt). Dr. Wakerlin and Dr. Rodbard advocated, respectively, the view that the primary stimulus might be the volume pulse or the transmural pressure in the renal arterial bed. An objection to renin as the cause of chronic hypertension based on tachyphylaxis experiments was raised by Dr. Findley. Dr. Goldblatt denied the presence of true tachyphylaxis and was supported by Drs. Helmer and Wakerlin. Dr. McCubbin suggested it might occur only with cruder preparations of renin, and Dr. Braun-Menéndez theorized that receptor sites might be occupied for a time after restoration of normal blood pressure, thus giving rise to a transient tachyphylaxis. Dr. Bumpus supported this explanation by reporting that a pressor response to crude angiotonin can sometimes not be maintained, while the response to pure angiotonin is persistent. Considerable discussion ensued between Drs. Goldblatt and Grollman concerning the mechanism of blood pressure reduction by removal of a single ischemic kidney. The human renal biopsy and autopsy studies suggesting the primacy of renal arteriolosclerosis in human hypertension were reviewed by Dr. Goldblatt.