Abstract
Surgical sympathetic decentralization does not alter the total or segmental renal vascular resistances measured 2 and 24 hours after the procedure regardless of the presence or absence of anesthesia. When the hematocrit ratio is raised from moderately anemic to moderately polycythemic levels by means of the infusion of washed red cell concentrates, the renal blood flow of the normal kidney is maintained while that of the denervated kidney diminishes. When account is taken of the increased blood viscosity incident to an elevated hematocrit, dilation is indicated at some point along the renal vascular circuit of the normal kidney. This failure of the blood flow to diminish in accordance with the elevation of blood viscosity cannot be explained by changes in the arterial pressure of the animal, as the average mean femoral pressure during the post-infusion periods was found to be only slightly elevated above the control level. Since in the normal kidney both the glomerular filtration rate and the filtration fraction were increased (the former moderately and the latter markedly), the average intraglomerular pressure of this kidney must have been increased, indicating the afferent arterioles as the primary point of dilation. This mechanism of preglomerular dilatation is the same one seen on a larger scale in experimental polycythemia, where the blood flow is greater than normal. Anesthesia and denervation impair the dilator mechanism in acute studies but no extrinsic nervous mechanism need be invoked to maintain renal blood flow in a chronic state of polycythemia. Since moderate changes in the hematocrit may bring about large changes in the filtration fraction, careful regard for this effect should be exercised in the interpretation of renal clearance data when the hematocrit is not controlled.