To determine if an increase in the endogenous secretion of parathyroid hormone could decrease sodium reabsorption by the proximal tubule, the ionized calcium concentration of blood perfusing the parathyroid gland of eight unilaterally thyroid parathyroidectomized dogs (TPTX) was reduced by infusion of an isotonic sodium citrate plus sodium chloride solution into the blood supply of the parathyroid gland. The fractional clearance of phosphate increased significantly (+9.3 +/- 2.8 ml/min per 100 ml GFR), while fractional sodium reabsorption by the proximal tubule decreased (-.06 +/- .02; P less than .025). In seven normal control dogs that received isotonic sodium chloride infusion, neither fractional sodium reabsorption by the proximal tubule nor the fractional clearance of phosphate was significantly altered. In five bilaterally TPTX dogs that received a sodium citrate plus sodium chloride infusion, sodium reabsorption by the proximal tubule was not significantly altered. There were no significant changes in glomerular filtration rate or renal plasma flow in any of these groups. The data demonstrate that alterations in endogenous parathyroid hormone secretion can play a significant role in the regulation of sodium reabsorption by the proximal tubule.

Effect of parathyroid hormone secretion on sodium reabsorption by the proximal tubule.

Southwestern Internal Medicine Conference: Renal Sodium Excretion and Atrial Natriuretic Factor

Renal lithium clearance in man : studies in normotensive and hypertensive subjects

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.

Regulation of glomerular filtration and proximal tubule reabsorption.

Isotonic reabsorption by the proximal tubule is mediated by an active transport process that is subject to physiologic control mechanisms. One school of thought proposes that the primary, and perhaps overriding, variables regulating proximal transport are physical factors (oncotic and hydrostatic pressures) in the peritubule environment. However, recent data indicate that membrane permeability is an important variable that must be considered when evaluating the regulatory role of physical factors. Such changes in membrane permeability could be the mechanism by which certain hormones regulate reabsorption by the proximal tubule. Hormones effecting sodium transport per se, such as aldosterone, do not have any effect on proximal reabsorption. However, hormones, such as parathyroid hormone, which have a primary effect on an anion reabsorption, specifically bicarbonate and phosphate, are effective in regulating proximal reabsorption. It is suggested that the physiologic regulation of isotonic reabsorption by the proximal tubule is mediated by hormonal regulation of these anions.

Role of physical and neuroendocrine factors in proximal electrolyte reabsorption.

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Role of physical and neuroendocrine factors in proximal electrolyte reabsorption.