Cyclic adenosine monophosphate-stimulated anion transport in rabbit cortical collecting duct. Kinetics, stoichiometry, and conductive pathways.

Schuster, Victor L.

doi:10.1172/jci112755

Cited by 47 publications

(29 citation statements)

References 33 publications

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“…Schuster and his co-worker (3,10) reported that cAMPinduced Cl-reabsorption in microperfused rabbit CCT was consistent with stimulation of an apical membrane Cl-conductance. We found that increasing intracellular cAMP levels by pretreatment with an adenyl cyclase activator, forskolin, or a cell-permeable cAMP analogue, db-cAMP, mimicked the stimulatory effect of PGE2 and increased 9-pS Cl-channel frequency in cell-attached patches by 7- ( 18).…”

Section: Discussionmentioning

confidence: 85%

“…Basolateral PGE2 in micromolar concentrations stimulates cAMP accumulation in freshly isolated and cultured rabbit CCT (12)(13)(14) and elevations in intracellular cAMP increase conductive C1-reabsorption in isolated rabbit CCT (3,10). Under basal conditions, 9-pS Cl-channel activity was observed in only 9% (11 / 126) of apical, principal cell-attached patches on rabbit CCT primary cultures (Fig.…”

Section: Resultsmentioning

confidence: 96%

“…cAMP is one candidate for the intracellular signaling pathway that regulates apical Cl -transport in the mammalian CCT. Elevation of intracellular cAMP increases conductive CF-reabsorption in isolated rabbit CCT (10). A variety of mechanisms might increase intracellular cAMP in CCT cells, but exposure to physiological concentrations of PGE2 stimu-lates cAMP accumulation in freshly isolated and cultured rabbit CCT (1 [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15].…”

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confidence: 99%

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Prostaglandin E2 activates clusters of apical Cl- channels in principal cells via a cyclic adenosine monophosphate-dependent pathway.

Ling¹,

Kokko²,

Eaton³

1994

J. Clin. Invest.

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IntroductionWe examined cell-attached patches on principal cells of primary cultured, rabbit cortical collecting tubules. Under basal conditions, apical 9-pS Cl --selective channels were observed in 9% of patches (11 / With its low baseline frequency and Ere, near resting membrane potential, this channel would not contribute significantly to transcellular Cl-flux under basal conditions. (e) However, cAMP-producing agonists (i.e., PGE2, arginine vasopressin) would increase apical C1-transport with the direction determined by the apical membrane potential. (J. Clin. Invest. 1994. 93:829-837.)

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Section: Discussionmentioning

confidence: 85%

Section: Resultsmentioning

confidence: 96%

mentioning

confidence: 99%

See 1 more Smart Citation

Prostaglandin E2 activates clusters of apical Cl- channels in principal cells via a cyclic adenosine monophosphate-dependent pathway.

Ling¹,

Kokko²,

Eaton³

1994

J. Clin. Invest.

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“…Intracellular cAMP is known to cause stimulation of AE activity in many cell types, 33 cholangiocytes included. 10,11,16 Thus, AE activity of silenced NRCs was also analyzed in the presence of the [cAMP] i stimulation mixture (cf.…”

Section: Effect Of Secretin On the Dids-sensitive CL ؊ / Hco 3 ؊ Exchmentioning

confidence: 99%

Bicarbonate-rich choleresis induced by secretin in normal rat is taurocholate-dependent and involves AE2 anion exchanger

et al. 2006

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Canalicular bile is modified along bile ducts through reabsorptive and secretory processes regulated by nerves, bile salts, and hormones such as secretin. Secretin stimulates ductular cystic fibrosis transmembrane conductance regulator (CFTR)-dependent Cl ؊ efflux and subsequent biliary HCO 3 ؊ secretion, possibly via Cl ؊ /HCO 3 ؊ anion exchange (AE). However, the contribution of secretin to bile regulation in the normal rat, the significance of choleretic bile salts in secretin effects, and the role of Cl ؊ /HCO 3 ؊ exchange in secretin-stimulated HCO 3 ؊ secretion all remain unclear. Here, secretin was administered to normal rats with maintained bile acid pool via continuous taurocholate infusion. Bile flow and biliary HCO 3 ؊ and Cl ؊ excretion were monitored following intrabiliary retrograde fluxes of saline solutions with and without the Cl ؊ channel inhibitor 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) or the Cl ؊ /HCO 3 ؊ exchange inhibitor 4,4 -diisothiocyanatostilbene-2,2 -disulfonic acid (DIDS). Secretin increased bile flow and biliary excretion of HCO 3 ؊ and Cl ؊ . Interestingly, secretin effects were not observed in the absence of taurocholate. Whereas secretin effects were all blocked by intrabiliary NPPB, DIDS only inhibited secretin-induced increases in bile flow and HCO 3 ؊ excretion but not the increased Cl ؊ excretion, revealing a role of biliary Cl ؊ /HCO 3 ؊ exchange in secretininduced, bicarbonate-rich choleresis in normal rats. Finally, small hairpin RNA adenoviral constructs were used to demonstrate the involvement of the Na ؉ -independent anion exchanger 2 (AE2) through gene silencing in normal rat cholangiocytes. AE2 gene silencing caused a marked inhibition of unstimulated and secretin-stimulated Cl ؊ /HCO 3 ؊ exchange. In conclusion, maintenance of the bile acid pool is crucial for secretin to induce bicarbonate-rich choleresis in the normal rat and that this occurs via a chloride-bicarbonate exchange process consistent with AE2 function. (HEPATOLOGY 2006;43:266-275.) S ecretin is known to induce bicarbonate-rich hydrocholeresis in many animal species. 1-7 Its interaction with a G-protein-coupled receptor selectively localized to the epithelial bile duct cells 8 results in increased intracellular levels of cyclic adenosine monophosphate (cAMP) [cAMP] i 7,9,10 and protein kinase A activation. 11,12 Phosphorylation and opening of a cAMP-dependent Cl Ϫ channel, the cystic fibrosis transmembrane conductance regulator (CFTR), 13 causes Cl Ϫ efflux to the ductular lumen. This appears to stimulate an apical Na ϩ -independent Cl Ϫ /HCO 3 Ϫ anion exchange (AE), 14 with HCO 3 Ϫ efflux and Cl Ϫ influx, that is facilitated by the outside to inside transmembrane gradient of Cl Ϫ at relatively high intracellular HCO 3 Ϫ concentration. [10][11][12]15,16 Several bicarbonate transporters, most of them encoded by the SLC4 and SLC26 gene families, 17 have been described to exert AE activity. A decade ago, we localized one of those polypeptides, the SLC4A2 or AE2, 18 to the apical membrane in...

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“…Wingo (25) Schuster (27) using cable analysis. In addition to these data from intact tubules, there is evidence that CFTRlike Cl-channels are present in the apical membrane of distal nephron cells.…”

Section: Controlmentioning

confidence: 99%

Anion secretion by the inner medullary collecting duct. Evidence for involvement of the cystic fibrosis transmembrane conductance regulator.

Husted¹,

Volk²,

Sigmund³

et al. 1995

J. Clin. Invest.

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It is well established that the terminal renal collecting duct is capable of electrogenic Na+ absorption. The present experiments examined other active ion transport processes in primary cultures of the rat inner medullary collecting duct. When the amiloride analogue benzamil inhibited electrogenic Na+ absorption, cAMP agonists stimulated a transmonolayer short circuit current that was not dependent on the presence of Na+ in the apical solution, but was dependent on the presence of Cl -and HCO -. This current was not inhibited by the loop diuretic bumetanide, but was inhibited by ouabain, an inhibitor of the Na+/K+ pump. The current was reduced by anion transport inhibitors, with a profile similar to that seen for inhibitors of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl-channel. Using several PCR strategies, we demonstrated fragments of the predicted lengths and sequence identity with the rat CFTR. Using whole-cell patch-clamp analysis, we demonstrated a cAMP-stimulated Cl -current with characteristics of the CFTR. We conclude that the rat inner medullary collecting duct has the capacity to secrete anions. It is highly likely that the CFTR Cl-channel is involved in this process. (J. Clin. Invest. 1995.95:644-650.)

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Cyclic adenosine monophosphate-stimulated anion transport in rabbit cortical collecting duct. Kinetics, stoichiometry, and conductive pathways.

Cited by 47 publications

References 33 publications

Prostaglandin E2 activates clusters of apical Cl- channels in principal cells via a cyclic adenosine monophosphate-dependent pathway.

Prostaglandin E2 activates clusters of apical Cl- channels in principal cells via a cyclic adenosine monophosphate-dependent pathway.

Bicarbonate-rich choleresis induced by secretin in normal rat is taurocholate-dependent and involves AE2 anion exchanger

Anion secretion by the inner medullary collecting duct. Evidence for involvement of the cystic fibrosis transmembrane conductance regulator.

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