Localization, mediation and function of the glomerular vascular response to alterations of distal fluid delivery

Abstract

Direct assessment of glomerular hemodynamics revealed that elevation of loop of Henle flow induces a significant increase of afferent arteriolar resistance. Examination of glomerular poles of normo- and hyperperfused nephrons by light microscopy supports this result by demonstrating significantly narrowed luminal diameters of afferent arterioles in the hyperperfused tubules. Thus, the decrease of glomerular filtration rate and glomerular capillary pressure induced by activating tubuloglomerular feedback is caused predominantly by vasoconstriction of the afferent arterioles. It is possible that the feedback-induced change of vasomotor tone is related to the action of locally generated angiotensin II. However, the pertinent experimental evidence does not appear to be internally consistent with this notion. Observations that methylxanthines, prostaglandin synthesis inhibitors, and beta-adrenergic blocking agents interfere with the initiation of normal feedback responses suggest that the vascular reaction is caused by a complex system of interdependent components. Constancy of nephron filtration rate during acute changes of arterial pressure is observed in rats when tubuloglomerular feedback is operative. In contrast, during acute and chronic interruption of feedback transmission, nephron GFR varies with blood pressure. While an intact feedback system is necessary for complete autoregulation of nephron GFR, calculation of the predicted dependency of GFR upon pressure reveals that some residual autoregulatory capacity remains even without a functional feedback system. It is concluded that, in addition to tubuloglomerular feedback, other mechanisms participate in GFR autoregulation.