AB STRA CT Electrical and permeability features of the distal convoluted tubule (DCT) and the cortical collecting tubule (CCT) were examined using the technique in which isolated segments of rabbit tubules were perfused in vitro. When rabbits were given a regular diet and tubules were perfused and bathed in artificial solutions simulating plasma ultrafiltrate, the potential difference (PD) was + 3.7+1.9 mV in the CCT and -40.4±2.8 mV in the DCT. When rabbits were given a low sodium, high potassium diet plus i.m. deoxycorticosterone acetate (DOCA) (1 mg/kg per day), the PD in both the CCT (-30.8±3.9 mV) and the DCT (-33.8±5.5 mV) was negative. The PD in the CCT was quantitatively similar to that of diet plus DOCA when animals were given DOCA alone. The PD in both segments was inhibited by ouabain (10' M) in the bath or by amiloride (10' M) in the perfusate. Addition of vasopressin (200 AU/ml) to the bath caused a gradual decline of PD to zero in the CCT but failed to produce a potential response in the DCT. Osmotic water permeability was essentially zero in both segments in the absence of vasopressin. After addition of the vasopressin to the bath, osmotic water permeability in the DCT remained zero but increased to 71.9+25.5 x 10-7 cm/s per atm in the CCT. We conclude that both segments are similar in that each possesses an electrogenic transport process but that these segments differ in that: (a) the CCT requires either exogenous or endogenous mineralocorticoid to maintain a maximal negative PD, whereas the PD in the DCT appears to be independent of mineralocorticoid effect; and (b) the CCT responds to vasopressin with a marked rise in water permeability, whereas the DCT is impermeable to water before and after addition of vasopressin.Dr. Imai's present address is the Department of Pharmacology, Jichi Medical School, Tochigi, Japan 329-04.

A B S T R A C T We have previously shown that the transtubular potential of the rabbit cortical collecting tubule varies in concert with changes in plasma mineralocorticoid levels, while the potential of the distal convoluted tubule is invariant with such changes. In the present studies we have examined the effects of in vitro addition of d-aldosterone to isolated tubules, as well as the effects of triamterene and spirolactone.d-Aldosterone (0.2 ,um added to the perfusate or 1 ,uM added to the bathing medium) resulted in a marked stimulation of the transtubular potential difference (lumen-negative) after a short latent period. d-Aldosterone had no effect on the potential difference of distal convoluted tubules of intact or adrenalectomized rabbits. Both the magnitude of the response and the length of the latent period in the cortical collecting tubule after aldosterone were markedly temperature-dependent. Triamterene cauised a gradual but reversible inhibition of the potential difference in the cortical collecting tubule but had no effect in the distal tubule. Spirolactone, when added before aldosterone, blocked the electrical response to the hormone in the cortical collecting tubule, and produced a gradual inhibition of the potential difference in mineralocorticoid-stimulated tubules. Spirolactone had no effect on the potential difference of the distal tubule.We conclude that (a) the influence of aldosterone on the potential across the distal nephron is restricted to the distal convoluted tubule, (b) the electrical response to aldosterone and the latent period are temperature-dependent, (c) the response to aldosterone is blocked by spirolactone, and (d) triamtereneReceivedfor publication 15 April 1976 and in revisedform 10 September 1976.

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The effect of tubular obstruction on renal function has been understood poorly at the tubular level and from the clinical standpoint. In our review the evidence for a direct influence of hydrostatic pressure on tubular transport and glomerular filtration is examined. The data generated to date indicate a direct influence of hydrostatic pressure on tubular transport only at the level of the distal convoluted tubule and collecting duct. With respect to glomerular filtration increased tubular pressure reduces the net driving force for filtration and reduces glomerular filtration rate in the absence of a compensatory increase in glomerular hydrostatic pressure. We next review physiological data concerning the mechanism of post-obstructive diuresis. Available information suggests 4 factors that play a significant role in the clinical syndrome of post-obstructive diuresis: 1) medullo-papillary washout, 2) decreased fractional and absolute salt and water reabsorption in the collecting duct, presumably secondary to direct influence of hydrostatic pressure on transport mechanisms, 3) osmotic diuresis secondary to retention of urea and other osmotic solutes during the period of obstruction and 4) prior salt and water administration in the absence of excretion, resulting in extracellular fluid volume expansion.