A functional comparison of the cortical collecting tubule and the distal convoluted tubule.

Gross, James B.; Imai, Masashi; Kokko, Juha P.

doi:10.1172/jci108048

Cited by 167 publications

(56 citation statements)

References 45 publications

(82 reference statements)

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“…In the salt-treated animals, there was a tendency for a higher FDNA% to the papillary base, although this difference was not statistically significant. These observations are in agreement with (12), loop of Henle (13), and distal convoluted tubule (1) have been shown to be relatively mineralocorticoid insensitive. Therefore, in our opinion, the most likely explanation is an enhanced sodium reabsorption by cortical and(or) medullary collecting tubules.…”

Section: Discussionsupporting

confidence: 90%

Collecting Duct Sodium Reabsorption in Deoxycorticosterone-Treated Rats

Haas¹,

Berndt²,

Youngberg³

et al. 1979

J. Clin. Invest.

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A B S T R A C T In vitro studies of isolated, perfused, cortical collecting tubules have demonstrated that prior chronic deoxycorticosterone acetate (DOCA) treatment increases sodium reabsorption in this nephron segment, yet sodium balance in vivo is maintained. To evaluate the effect of chronic DOCA treatment on collecting duct sodium reabsorption in vivo, we compared fractional sodium delivery (FDNa%) out of the superficial late distal tubule with the fraction of sodium remaining at the base and the tip of the papillary collecting duct during extracellular fluid volume expansion in untreated, salt-treated, and DOCA-salt-treated rats. In untreated rats, FDNa% to the distal tubule was 6.5+1.0%, and to the base was 8.7+1.6% (A 2.2+0.9%, P < 0.05). FDNa% to the tip was 4.9+ 1.1%, significantly less than FDNa% to the base (A 3.7±1.1%, P < 0.01). In salt-treated rats, FDNa% to the distal tubule was 8.3±0.8%, and to the base was 10.4±1.1%. FDNa% to the tip was 5.9±0.6%, significantly less than FDNa% to the base (A 4.6+ 1.0%, P < 0.005). In DOCA-salttreated rats, FDNa% to the distal tubule was 16.1±2.6% and to the base was 9.5±1.9% (A 6.6±1.7%, P < 0.005). FDNa% to the tip was 5.9±1.2%, also significantly less than FDNa% to the base (A 3.6±1.1%, P < 0.01). We conclude that (a) in DOCA-salt-treated rats, sodium delivery to the end of the superficial distal tubule is greater than in untreated or salt-treated rats; (b) in DOCA-salt-treated rats, sodium delivery to the end of the superficial distal tubule is greater than to the base of the papillary collecting duct, suggesting stimulation of sodium reabsorption in the cortical and(or) outer medullary collecting duct; and (c) sodium reabsorption by the papillary collecting duct is unaffected by chronic DOCA-salt treatment in the volume-expanded rat.

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Section: Discussionsupporting

confidence: 90%

Collecting Duct Sodium Reabsorption in Deoxycorticosterone-Treated Rats

Haas¹,

Berndt²,

Youngberg³

et al. 1979

J. Clin. Invest.

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“…This meneuver was done to insure a transepithelial potential difference (PD) lumen negative (2). All animals had free access to food and water before guillotine decapitation.…”

Section: Methodsmentioning

confidence: 99%

“…The PD of CCT from normal rabbits is difficuilt to predict and is dependent, at least in part, on the mineralocorticoid activity (2). The administration of DOCA insures a negative PD which is invariably responsive to PGE2 in doses of 0.1 ,M or greater.…”

Section: Methodsmentioning

confidence: 99%

“…This work was presented, in part, at the 9th Annual Meeting of the American Society of Nephrology, [21][22][23] November is the segment sensitive to aldosterone (2,3) and in this way is capable of regulating sodium reabsorption. Rapid natriuresis in response to a variety of stimuli such as acute volume expansion cannot be explained fully by inhibition of aldosterone because of its long duration of action.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of sodium transport by prostaglandin E2 across the isolated, perfused rabbit collecting tubule.

Stokes¹,

Kokko²

1977

J. Clin. Invest.

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348

151

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A B S T RAC T This study was designed to examine whether prostaglandin E2 can directly affect sodium transport across isolated perfused rabbit renal collecting tubules. Changes in transepithelial potential and isotopic sodium fluxes in response to peritubular prostaglandin E2 were measured. In addition, changes in transepithelial potential of the outer medullary collecting tubule in response to prostaglandin E2 were also measured. With few exceptions, all rabbits received 5 mg/day desoxycorticosterone acetate for 4-11 days before experimentation. The results ofthe experiments show that: (a) prostaglandin E2 inhibits the negative transepithelial potential in the cortical collecting tubule as well as the outer medullary collecting tubule; (b) prostaglandin E2 inhibits net sodium transport out of the lumen by inhibiting efflux while backflux is unaffected; (c) prostaglandin E2 produces this inhibition within 15 min, and the effects are dose dependent and reversible. These results suggest that prostaglandin E2 may modulate sodium transport in vivo and may contribute to the final regulation of sodium excretion.

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“…There have been studies examining the direct effect of in vitro increases in hydrostatic pressure on tubular function in isolated perfused tubules. They demonstrated that an acute in vitro increase in hydrostatic pressure has no effect on proximal convoluted tubule fluid reabsorption (11) but may alter transport in the cortical collecting tubule since the potential difference fell in response to this maneuver (12). The lack of information on intrinsic tubular function following relief of obstruction prompted us to develop a model of unilateral ureteral obstruction (UUO) and bilateral ureteral obstruction (BUO) for 24 h in the New Zealand White rabbit (13 …”

Section: Introductionmentioning

confidence: 99%