Abstract

In this review current hypotheses for the regulation of filtration rate and the subsequent reabsorption of that filtrate by the proximal tubule are discussed. In the rat the filtration rate is highly plasma flow dependent because of the phenomenon of filtration equilibrium. On the other hand, in man and dog filtration rate is much less dependent on renal plasma flow. In these species glomerular capillary pressure rather than glomerular plasma flow may be the primary determinant of filtration. Three hypotheses for the autoregulation of glomerular filtration are discussed. Of these the myogenic theory, which holds that increases in perfusion pressure result in an intrinsic contraction of the smooth muscle in the walls of the afferent arterioles, remains the best, if not completely adequate, explanation for the phenomenon. The role of a macula densa feedback mechanism is controversial, although data are presented which strongly militate against this hypothesis. Similarly, the prostaglandins, although important in determining vascular resistance, probably do not mediate autoregulation. Two prevalent hypotheses for the regulation of fluid reabsorption by the proximal tubule, the physical factor hypothesis and the humoral hypothesis, are discussed. Data presented indicate that peritubule Starling forces have a marked effect on isotonic reabsorption by the proximal tubule in the presence of volume expansion and enhanced backleak into the proximal tubule lumen. However, in hydropenia and diminished backleak, changes in peritubule capillary Starling forces have little effect on proximal sodium reabsorption. Thus, the physical factor mechanism is a rather insensitive regulator of proximal reabsorption in the absence of volume expansion. Hormones known to regulate sodium transport per se, such as aldosterone, have no effect on sodium reabsorption by the proximal tubule. In contrast, those hormones primarily regulating anion reabsorption in the proximal tubule, such as parathyroid hormone, have significant effects on fluid reabsorption. Thus, the humoral regulation of anion reabsorption has secondary effects on proximal sodium reabsorption.

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