Abstract
Using his previously developed formulae for measuring afferent and efferent arteriolar resistance of human kidneys, based on clinical detns. of blood pressure, hematocrit, and diodrast and inulin clearances, the author analyzes the renal data reported by Homer Smith and his collaborators for adrenalin ischemia, pyrogenic hyperemia, and the basal state in normal human subjects. Where the range among many individuals of inulin clearance (rate of glomerular filtration) per unit functional kidney (diodrast tubular mass of Homer Smith) is reported relatively constant, both afferent and efferent arterioles are active in causing the change of resistance from renal ischemia to hyperemia. At the mean basal state, a 1% decrease in renal blood flow is caused by a 0.2% decrease in afferent arteriolar resistance and a 0.9% increase in efferent arteriolar resistance. The significance of postulating that the fall in blood pressure in the efferent arterioles is inversely proportional to the flow through them is to postulate that efferent arterioles modify their resistance so that the heat produced by the friction of the blood flowing through them remains constant. This hypothesis, on examination by means of the formulae, is untenable.