Properties and Diversity of (Na-K-C1) Cotransporters

Haas, Mark

doi:10.1146/annurev.ph.51.030189.002303

Cited by 220 publications

(93 citation statements)

References 51 publications

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“…2). We have previously used [ 3 H]BSTBA photolabeling to identify Na-K-Cl cotransport proteins of other tissues, including dog and mouse kidney, duck red blood cells, and shark rectal gland (32)(33)(34). In each case, the molecular mass of the protein identified by [ 3 H]BSTBA labeling was subsequently found to be in excellent agreement with that determined by Western blotting using anti-cotransporter antibodies (14,34).…”

Section: Resultsmentioning

confidence: 69%

[Cl-]i-dependent Phosphorylation of the Na-K-Cl Cotransport Protein of Dog Tracheal Epithelial Cells

Haas¹,

McBrayer²,

Lytle³

1995

Journal of Biological Chemistry

105

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Basolateral Na-K-Cl cotransport activity in primary cultures of dog tracheal epithelial cells is stimulated by ␤-adrenergic agents, such as isoproterenol, and by apical UTP, which acts through an apical P 2 -purinergic receptor. While at least part of the stimulatory effect of isoproterenol appears to involve direct activation of the cotransporter via cAMP-dependent protein kinase, cotransport stimulation by apical UTP is entirely secondary to apical Cl

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Section: Resultsmentioning

confidence: 69%

[Cl-]i-dependent Phosphorylation of the Na-K-Cl Cotransport Protein of Dog Tracheal Epithelial Cells

Haas¹,

McBrayer²,

Lytle³

1995

Journal of Biological Chemistry

105

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“…Na-K+-2Cl-cotransporters are found in a wide variety of cell types (1,2). This transport system is thought to play a central role in salt and water movements in many absorptive and secretory epithelia.…”

Section: Introductionmentioning

confidence: 99%

“…It is also involved in volume regulatory phenomena in both epithelial and nonepithelial cells. As is characteristic of other transporters that are extensively utilized in nature, Na+-K+-2Cl-cotransport activity is regulated in a very tissue-specific manner (1,2). Thus, in some cell types, increases in cyclic nucleotide levels, intracellular calcium concentration, or protein kinase C activity stimulate the cotransporter, whereas in others, these same agents may have exactly the opposite effect, or possibly no effect at all.…”

Section: Introductionmentioning

confidence: 99%

Beta-adrenergic upregulation of the Na(+)-K(+)-2Cl- cotransporter in rat parotid acinar cells.

Paulais¹,

Turner²

1992

J. Clin. Invest.

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We used the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6')-carboxyfluorescein to monitor the recovery of the intracellular pH (pH,) of rat parotid acini from an NH+-induced alkaline load. This recovery was markedly inhibited by the loop diuretic bumetanide and by Cl-removal, indicating that it is largely due to NH' entry via the basolateral Na'-K+-2Cl-cotransporter. The rate of recovery of pHi was enhanced threefold by pretreatment (37.5 s) with isoproterenol (K112 = 21.5 nM) or norepinephrine (in the presence of phentolamine), and blocked by the #,-specific antagonist atenolol, indicating an upregulation of cotransport activity by ,81-adrenergic stimulation. The effect of isoproterenol was prevented by protein kinase inhibitors and mimicked by cAMP analogues, and by maneuvers known to increase cytosolic cAMP levels in these cells, consistent with the involvement ofprotein kinase A. Physiologically, such an upregulation of the acinar Na'-K+-2CI-cotransporter would lead to an increase in acinar chloride uptake across the basolateral membrane, and consequently, an increase in overall chloride and fluid secretion. Prevention of this upregulation by t-blockers and possibly by other commonly used clinical agents may account for the dry mouth and dry eyes experienced by some patients taking these medications. (J.

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“…The Malpighian tubules of A. domesticus are relatively insensitive to the loop diuretics bumetanide and furosemide, but they reduce secretion by almost 70%, and bumetanide has no effect on V b , which is consistent with the coupled uptake of Na (16) cotransport (Haas, 1989;Gamba et al, 1994 (Gamba et al, 1993), which mimics the effect of bumetanide on cricket tubules, and bumetanide reduces both Na + and K + transport, rather than just Na + transport. In addition, the diuretic activity of Achdo-DH, a corticotrophin releasing factor (CRF)-related peptide, has been shown to require Na (Payne and Forbush, 1995;Coast et al, 2002).…”

Section: Ion Transport Across the Basolateral Membranementioning

confidence: 66%

Intracellular Na+, K+ and Cl− activities in Acheta domesticus Malpighian tubules and the response to a diuretic kinin neuropeptide

Coast

2012

Journal of Experimental Biology

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SUMMARY The mechanism of primary urine production and the activity of a diuretic kinin, Achdo-KII, were investigated in Malpighian tubules of Acheta domesticus by measuring intracellular Na+, K+ and Cl− activities, basolateral membrane voltage (Vb), fluid secretion and transepithelial ion transport. Calculated electrochemical gradients for K+ and Cl− across the basolateral membrane show they are actively transported into principal cells, and basolateral Ba2+-sensitive K+ channels do not contribute to net transepithelial K+ transport and fluid secretion. A basolateral Cl− conductance was revealed after the blockade of K+ channels with Ba2+, and a current carried by the passive outward movement of Cl− accounts for the hyperpolarization of Vb in response to Ba2+. Ion uptake via Na+/K+/2Cl− cotransport, driven by the inwardly directed Na+ electrochemical gradient, is thermodynamically feasible, and is consistent with the actions of bumetanide, which reduces fluid secretion and both Na+ and K+ transport. The Na+ gradient is maintained by its extrusion across the apical membrane and by a basolateral ouabain-sensitive Na+/K+-ATPase. Achdo-KII has no significant effect on the intracellular ion activities or Vb. Electrochemical gradients across the apical membrane were estimated from previously published values for the levels of Na+, K+ and Cl− in the secreted fluid. The electrochemical gradient for Cl− favours passive movement into the lumen, but falls towards zero after stimulation by Achdo-KII. This coincides with a twofold increase in Cl− transport, which is attributed to the opening of an apical Cl− conductance, which depolarises the apical membrane voltage.

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Properties and Diversity of (Na-K-C1) Cotransporters

Cited by 220 publications

References 51 publications

[Cl-]i-dependent Phosphorylation of the Na-K-Cl Cotransport Protein of Dog Tracheal Epithelial Cells

[Cl-]i-dependent Phosphorylation of the Na-K-Cl Cotransport Protein of Dog Tracheal Epithelial Cells

Beta-adrenergic upregulation of the Na(+)-K(+)-2Cl- cotransporter in rat parotid acinar cells.

Intracellular Na+, K+ and Cl− activities in Acheta domesticus Malpighian tubules and the response to a diuretic kinin neuropeptide

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