Glomerulotubular balance (GTB) is defined as the ability of each successive segment of the proximal tubule to reabsorb a constant fraction of glomerular filtrate and solutes delivered to it. For maintenance of GTB the coupling of peritubular blood flow and intratubular fluid flow to the process of glomerular filtration seems to be of functional importance since tubular fluid reabsorption is significantly altered when either or both parameters are experimentally changed. In the case of peritubular blood flow, variations of tubular fluid reabsorption have been ascribed to variations of the mean net colloid osmotic pressure in the peritubular blood and its effects on the paracellular backleak of tubular resorbate. This relationship has, however, been clearly demonstrated only in volume expansion, when GTB is impaired. Under nondiuretic conditions, in which GTB typically occurs, the importance of the peritubular colloid osmotic pressure in control of tubular fluid reabsorption is less clear since variations of peritubular colloid osmotic pressure within a physiologic range exert only a negligible influence on tubular fluid transport. Pharmacologically induced alterations of peritubular hemodynamics or mean net colloid osmotic pressure can affect tubular fluid reabsorption without consistently altering the net interstitial pressure. In the case of intratubular flow rate, variations of tubular fluid reabsorption are comparable to changes seen with GTB. Such an interrelation is found only in tubules perfused by natural tubular fluid. In individual nephrons flow-dependent reabsorption cannot always be observed even when it appears that GTB is preserved in that kidney. Flow dependency of tubular fluid reabsorption might be attributed to some properties or constituents in tubular fluid rather than to some intrinsic characteristics of the tubular epithelium. Because flow dependence and tubular fluid transport are homogeneous along the tubule, fluid reabsorption might be controlled by a mechanism akin to a flow reactor. As yet it is not possible to explain GTB exclusively by peritubular or luminal control alone.

In hydropenic rats, the reabsorption of glomerular filtrate by the proximal convoluted tubules was measured before and after reduction of its intratubular flow rate. Three different protocols were used. (1) In 26 tubules (14 rats), nephron glomerular filtration rate (SNGFR) was varied from 37.2 +/- 7.3 to 20.4 +/- 7.1 nl/min by microperfusing their loops of Henle at 0 to 5 nl/min and 40 nl/min, respectively. This 43% reduction of SNGFR was followed by a 36.0 +/- 23.3% reduction of volume reabsorption rate (P less than 0.001). Between both parameters a linear regression line can be calculated, which is given by y = 0.92 chi + 0.0017. (2) In 17 tubules (14 rats), SNGFR was altered again by feedback from 46.0 +/- 9.7 to 28.8 +/- 9.3 nl/min. The volume resorption from the first half of the proximal convoluted tubule was compared with the reabsorption in its late proximal segments, which were microperfused with proximal tubular fluid at a rate of 20 nl/min. The 36.8% reduction of SNGFR was followed by only a 28.2% reduction of volume reabsorption rate in the first half of the tubule. In the microperfused segments, however, reabsorption remained unaltered. (3) In 29 tubules (21 rats), at the midpoint of proximal convolutions, some of the tubule fluid was removed by a suction pump, and volume reabsorption rate in the late segments was compared with that in the early parts of this tubule, when SNGFR remained stable. The reduction of intratubular flow from 27.7 +/- 8.5 to 14.7 +/- 5.8 nl/min, which is 53% of control, were followed by a reduction of volume reabsorption rate in the late segment to 60.6% control. Between both parameters a regression line was calculated, which is given by y = 0.76 chi +/- 0.01. We conclude that the rate of volume reabsorption by the proximal tubule depends on its intratubular load of glomerular filtrate and, further, that this dependency accounts predominantly for the maintenance of glomerular tubular balance under conditions of hydropenia.

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Experiments were performed to qualitatively characterize the effects of tubuloglomerular feedback (TGF) inhibition by chronic salt loading on salt sensitivity of blood pressure in spontaneously hypertensive rats (SHR). After two weeks of salt loading, systolic blood pressure (SBP) was significantly exacerbated and plasma volume (PV) was expanded in salt-loaded SHR compared with those in control SHR (SBP: 182 +/- 1 vs. 159 +/- 2 mm Hg; PV: 4.38 +/- 0.06 vs. 4.04 +/- 0.03 ml/100 g body wt, respectively). Plasma volume of WKY was also but only transiently expanded by salt loading, whereas plasma volume expansion in SHR had persisted over the entire dietary treatment period. TGF activity was assessed as the maximal reduction of single nephron GFR (SNGFR) on increasing loop of Henle perfusion rate from 0 to 40 nl/min using previously collected tubular fluid from salt-loaded rats (TFs) or control rats (TFc). Maximal TGF response in salt-loaded SHR with TFs was 14.9 +/- 2.9% and 57.8 +/- 2.6% with TFc. In control SHR the responses were 16.9 +/- 2.5% with TFs and 52.7 +/- 2.9% with TFc. In salt-loaded WKY the response with TFs were 3.1 +/- 1.6% and 37.4 +/- 2.8% with TFc. And in control WKY, the response with TFs were 8.2 +/- 1.9% and 40.8 +/- 2.8% with TFc, respectively. These results indicate the TGF resetting in chronically salt-loaded SHR and WKY is caused by the activation of humoral TGF inhibitory factor. The suppression of TGF in SHR was, however, far more variable and, on average, less than in WKY.(ABSTRACT TRUNCATED AT 250 WORDS)