Several factors are potentially able to change the glomerular filtration rate (GFR) and thereby participate in its regulation, but only a few factors seem to be physiologically important. The variable nature of proximal tubular pressure should be recognized as important in the regulation of GFR. It is argued that a distinction should be made between the terms 'autoregulation of GFR' and 'regulation of GFR'. The tubuloglomerular feedback mechanism (TGF) is an important factor for autoregulatory control of GFR. When perturbations result in major increases in tubular flow, the TGF saturates. Proximal tubular pressure then increases and becomes the major factor responsible for the stabilization of GFR. Changes in the proximal reabsorption rate (APR) are important for long-term variations in GFR (regulation of GFR). Small changes in the APR cause near parallel changes in the GFR mainly through the TGF mechanism, while larger changes in the APR cause near parallel changes in the GFR mainly because of the effect on tubular pressure. The hydraulic resistance in the distal nephron segments is an additional factor in regulating GFR, through its effect on proximal tubular pressure. The stimulus to the TGF mechanism also depresses renin release. The resulting local angiotensin II concentration has effects both on the arteriolar resistances and on the APR. The renin-angiotensin system and TGF are therefore considered to be integrated parts of a common control system regulating GFR. According to the hypothesis advocated here, TGF-mediated changes in afferent arteriolar resistance and angiotensin-mediated changes in efferent arteriolar resistance and APR cooperate in counteracting perturbations in proximal tubular pressure and Henle loop flow. However, because of the biphasic proximal effect of angiotensin II, a major unresolved question is whether physiological increases in endogenous local angiotensin II concentrations stimulate or inhibit proximal reabsorption.

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In rats on a diet with a sodium content of 300 mmol/kg, lithium is reabsorbed exclusively in the proximal tubules, and lithium clearance (CLi) equals the proximal tubular fluid output (Vprox). In rats on a sodium-poor diet (5 mmol/kg), lithium is also reabsorbed in the distal nephron and CLi is therefore lower than Vprox. The present paper examines the reduction of CLi in response to a low sodium diet in Brattleboro rats with hereditary diabetes insipidus maintained on different dietary potassium contents. CLi was reduced by about 60 microliter/min./100 g body weight in response to a low sodium diet. The absolute reduction in CLi caused by low sodium diet was unaffected by an increase of CLi provoked by administration of potassium with the diet, and it was unaffected by variations of CLi which occurred spontaneously within each group. CLi was accordingly reduced by a constant absolute value rather than by a constant percentage. The reduction of CLi (60 microliter/min./100 g body weight) was equal to CLi in the group given a potassium-poor diet with a normal sodium content. In the low-sodium and low-potassium group CLi was reduced to almost zero. Using CLi as a measure of Vprox in the rats on a 300 mmol/kg sodium diet it is concluded that the absolute reduction of CLi in response to a sodium-poor diet is 1) unaffected by increase of Vprox produced by administration of potassium with the food,2) unaffected by spontaneous variations of Vprox, and 3) equal to Vprox in rats given a potassium-poor diet.

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