Effects of protein kinase C activation on sodium, potassium, chloride, and total CO2 transport in the rabbit cortical collecting tubule.

Hays, Steven R.; Baum, Michel; Kokko, Juha P.

doi:10.1172/jci113242

Cited by 64 publications

(38 citation statements)

References 46 publications

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“…Several studies have shown that direct PKC stimulation and hormones acting via PKC stimulation decrease the activity of the amiloride-sensitive epithelial sodium channel and hence sodium reabsorption in the cortical collecting duct and A6 epithelia (Yanase and Handler, 1986;Hays et al, 1987;Ling and Eaton, 1989;Ling et al, 1992;Takeda et al, 1994;Frindt et al, 1996). In the present study, we confirm that PKC stimulation by PMA blocks the amiloride-sensitive short circuit current in A6 epithelia while it stimulates an amiloride-resistant ISc, which most likely corresponds to Cl secretion ( Figure 1; Yanase and Handler, 1986).…”

Section: Effect Of Pkc Stimulation On Sodium Reabsorptionsupporting

confidence: 84%

“…Transepithelial sodium reabsorption in the kidney cortical collecting duct has been shown to be decreased following PKC activation (Hays et al, 1987), and the decrease in sodium channel activity induced by high intracellular sodium (feedback regulation; Frindt et al, 1996), acetylcholine (Takeda et al, 1994), or prostaglandin E2 (Ling et al, 1992) is mediated by PKC activation. A similar role for PKC in sodium channel regulation by sodium feedback and prostaglandin E2 has been described in X. laevis A6 cells that are used as a model for cortical collecting duct principal cells (Ling and Eaton, 1989;Eaton et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

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Phorbol 12-myristate 13-acetate down-regulates Na,K-ATPase independent of its protein kinase C site: decrease in basolateral cell surface area.

Beron

Forster

Béguin

et al. 1997

MBoC

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The effect of protein kinase C (PKC) stimulation on the pump current (Up) generated by the Na,K-ATPase was measured in A6 epithelia apically permeabilized with amphotericin B. Phorbol 12-myristate 13-acetate (PMA) produced a decrease in I carried by sodium pumps containing the endogenous Xenopus laevis or transfected BuJ'o marinus al subunits (-30% reduction within 25 min, maximum after 40 min) independent of the PKC phosphorylation site (T15A/S16A). In addition to this major effect of PMA, which was independent of the intracellular sodium concentration and was prevented by the PKC inhibitor bisindolylmaleimide GF 109203X (BIM), another BIM-resistant, PKC siteindependent decrease was observed when the Ip was measured at low sodium concentrations (total reduction -50% at 5 mM sodium). Using ouabain binding and cell surface biotinylation, stimulation of PKC was shown to reduce surface Na,K-ATPase by 14 to 20% within 25 min. The same treatment stimulated fluid phase endocytosis sevenfold and decreased by 16.5% the basolateral cell surface area measured by transepithelial capacitance measurements. In conclusion, PKC stimulation produces a decrease in sodium pump function which can be attributed, to a large extent, to a withdrawal of sodium pumps from the basolateral cell surface independent of their PKC site. This

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Section: Effect Of Pkc Stimulation On Sodium Reabsorptionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Phorbol 12-myristate 13-acetate down-regulates Na,K-ATPase independent of its protein kinase C site: decrease in basolateral cell surface area.

Beron

Forster

Béguin

et al. 1997

MBoC

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“…In the presence of IO-sM amiloride in the lumen, ACh did not change VT, VB, and fRA (Table II (Fig. 1) inhibited Na' reabsorption in the rabbit CCD (25). It has been also reported that PGE2 inhibits the apical Na' channel via the PKC pathway (26).…”

Section: Resultsmentioning

confidence: 77%

Inhibition of amiloride-sensitive apical Na+ conductance by acetylcholine in rabbit cortical collecting duct perfused in vitro.

Takeda

Yoshitomi²,

Taniguchi³

et al. 1994

J. Clin. Invest.

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We examined effects of acetylcholine (ACh) on the electrical parameters and intracellular Ca2" concentration (ICa2+I) in the isolated rabbit cortical collecting duct (CCD) perfused in vitro using the conventional microelectrode technique and microscopic fluorescence spectrophotometry. ACh (10-8 to 1j-5 M) in the bath caused a positive deflection of the transepithelial voltage (VT) and an increase in ICa2"Ji. Carbachol also showed similar but smaller effects. The effects of ACh were antagonized by muscarinic receptor antagonists. ACh at 106 M hyperpolarized the apical membrane voltage and increased the fractional resistance of the apical membrane of the collecting duct cells accompanied by a positive deflection of V T and an increase in transepithelial resistance, whereas it did not affect these parameters in the a-intercalated cells. In the presence of 10-5 M amiloride in the lumen, the effects of ACh were almost completely abolished. The ACh-induced increase in [Ca2+]i is accounted for by the release of Ca2" from intracellular store and Ca2" entry from the bath. In the absence of Ca2" in the bath, the ACh-induced changes in electrophysiological parameters were significantly smaller than those observed in the presence of Ca2". Both phorbol-12-myristate-13-acetate (PMA) and phorbol-12,13-dibutylate (PDBu), activators of protein kinase C (PKC), also inhibited the apical Na+ conductance. In the presence of PMA or PDBu in the bath, ACh did not show further inhibitory effect. 1-(5-Isoquinolinylsulfonyl)-2-methylpiperazine, an inhibitor of PKC, partially attenuated the effect of ACh. These observations indicate that ACh inhibits the apical Na+ conductance partly by both increasing [Ca2+j] and activating PKC. Such an action of ACh may partially explain its natriuretic effect. (J. Clin. Invest. 1994. 93:2649-2657

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“…A PKC-dependent AQP2 retrieval from apical membrane of principal cells has also been observed (56). Other studies suggest that calcium/PKC-coupled signaling not only inhibits water flow but also inhibits Na ϩ absorption and K ϩ secretion in the collecting ducts (26,46,59).…”

Section: Discussionmentioning

confidence: 85%

Axial heterogeneity of vasopressin-receptor subtypes along the human and mouse collecting duct

Carmosino¹,

Brooks²,

Cai³

et al. 2007

American Journal of Physiology-Renal Physiology

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Vasopressin and vasopressin antagonists are finding expanded use in mouse models of disease and in clinical medicine. To provide further insight into the physiological role of V1a and V2 vasopressin receptors in the human and mouse kidney, intrarenal localization of the receptors mRNA was determined by in situ hybridization. V2-receptor mRNA was predominantly expressed in the medulla, whereas mRNA for V1a receptors predominated in the cortex. The segmental localization of vasopressinreceptor mRNAs was determined using simultaneous in situ hybridization and immunohistochemistry for segment-specific markers, including aquaporin-2, Dolichos biflorus agglutinin, epithelial Na channels, Tamm Horsfall glycoprotein, and thiazide-sensitive Na ϩ -Cl Ϫ cotransporter. Notably, V1a receptor expression was exclusively expressed in V-ATPase/anion exchanger-1-labeled alpha-intercalated cells of the medullary collecting duct in both mouse and human kidney. In cortical collecting ducts, V1a mRNA was more widespread and detected in both principal and intercalated cells. V2-receptor mRNA is diffusely expressed along the collecting ducts in both mouse and human kidney, with higher expression levels in the medulla. These results demonstrate heterogenous axial expression of both V1a and V2 vasopressin receptors along the human and mouse collecting duct. The restricted expression of V1a-receptor mRNA in intercalated cells suggests a role for this receptor in acid-base balance. These findings further suggest distinct regulation of renal transport function by AVP through V1a and V2 receptors in the cortex vs. the medulla. in situ hybridization; vasopressin receptors; intercalated cell ARGININE VASOPRESSIN (AVP) is the key hormone responsible for producing a concentrated urine and is secreted in high concentrations during antidiuresis. At least two different vasopressin

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Effects of protein kinase C activation on sodium, potassium, chloride, and total CO2 transport in the rabbit cortical collecting tubule.

Cited by 64 publications

References 46 publications

Phorbol 12-myristate 13-acetate down-regulates Na,K-ATPase independent of its protein kinase C site: decrease in basolateral cell surface area.

Phorbol 12-myristate 13-acetate down-regulates Na,K-ATPase independent of its protein kinase C site: decrease in basolateral cell surface area.

Inhibition of amiloride-sensitive apical Na+ conductance by acetylcholine in rabbit cortical collecting duct perfused in vitro.

Axial heterogeneity of vasopressin-receptor subtypes along the human and mouse collecting duct

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