Role of protein kinase C in aldosterone-induced non-genomic inhibition of basolateral potassium channels in human colonic crypts

Bowley, Kate A.; Linley, John E.; Robins, Gerrard G.; Kopanati, S; Hunter, Malcolm; Sandle, Geoffrey I.

doi:10.1016/j.jsbmb.2006.10.003

Cited by 7 publications

(2 citation statements)

References 32 publications

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“…Electrophysiological studies have localized K + efflux from this channel to the basolateral membrane of epithelial cells (Bleich et al. , 1996; Bowley et al. , 2007) as well as the apical membrane (Joiner et al.…”

Section: Introductionmentioning

confidence: 99%

Loss of Ca²⁺‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca²⁺‐activated K⁺ channel opener

Hirota

McKay

2009

British J Pharmacology

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Background and purpose: Epithelial surface hydration is critical for proper gut function. However, colonic tissues from individuals with inflammatory bowel disease or animals with colitis are hyporesponsive to Cl -secretagogues. The Cl -secretory responses to the muscarinic receptor agonist bethanechol are virtually absent in colons of mice with dextran sodium sulphate (DSS)-induced colitis. Our aim was to define the mechanism underlying this cholinergic hyporesponsiveness.

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Section: Introductionmentioning

confidence: 99%

Loss of Ca²⁺‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca²⁺‐activated K⁺ channel opener

Hirota

McKay

2009

British J Pharmacology

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“…ATP-dependent K + channel (K ATP ) activity in A6 CCD renal cells was rapidly stimulated by aldosterone (15 min), and this activation modulated the open probability of the channel [21]. Aldosterone has also been shown to produce a non-genomic inhibition of Ca 2+ -dependent intermediate conductance channels (IK Ca ) located in the basolateral membrane of colonic crypt cells, and this effect was PKC-dependent [40,41]. Additionally, aldosterone can also activate Na + /H + exchange through Ca 2+and PKC-dependent signaling pathways that results in an upregulation of K ATP and an inhibition of IKCa channels [42].…”

Section: Genomic and Non-genomic Actions Of Aldosterone On Epithelialmentioning

confidence: 99%

Aldosterone Regulation of Protein Kinase Signaling Pathways and Renal Na⁺Transport by Non-genomic Mechanisms

Thomas¹,

Harvey²

2019

Aldosterone-Mineralocorticoid Receptor - Cell Biology to Translational Medicine

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Aldosterone is the key regulating hormone of whole-body fluid and electrolyte homeostasis. Perturbations in aldosterone synthesis and over-activation of the mineralocorticoid receptor (MR) can lead to excess salt reabsorption and hypertension. The cortical collecting duct (CCD) is the main site of action in the kidney for aldosterone regulation of whole-body sodium homeostasis through actions on the epithelial sodium channel (ENaC) and the Na/K-ATPase (Na/K pump). Aldosterone stimulates ENaC trafficking into the apical cell membranes in the CCD and enhances channel stability and open probability, as well as activating the basolateral membrane Na/K pump to produce an overall increase in the transepithelial reabsorption of sodium. Aldosterone/MR regulates the activity of ENaC in the CCD through both rapid non-genomic (secs-mins) and latent genomic (hours-days) signaling pathways. These rapid and slow responses of renal Na + transport pathways to aldosterone are often treated as distinct and separate events. However, recent evidence points to a close integration between genomic and non-genomic responses to aldosterone to regulate ENaC and Na/K pump activity via protein kinase signaling pathways. Here, we review the integration of aldosterone membrane-initiated non-genomic and nuclear genomic regulations of renal sodium transport via protein kinase signaling pathways and in particular via protein kinase D isoforms.

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Protein kinase C

2009

Class 2 Transferases

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Role of protein kinase C in aldosterone-induced non-genomic inhibition of basolateral potassium channels in human colonic crypts

Cited by 7 publications

References 32 publications

Loss of Ca²⁺‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca²⁺‐activated K⁺ channel opener

Loss of Ca²⁺‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca²⁺‐activated K⁺ channel opener

Aldosterone Regulation of Protein Kinase Signaling Pathways and Renal Na⁺Transport by Non-genomic Mechanisms

Protein kinase C

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Role of protein kinase C in aldosterone-induced non-genomic inhibition of basolateral potassium channels in human colonic crypts

Cited by 7 publications

References 32 publications

Loss of Ca2+‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca2+‐activated K+ channel opener

Loss of Ca2+‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca2+‐activated K+ channel opener

Aldosterone Regulation of Protein Kinase Signaling Pathways and Renal Na+Transport by Non-genomic Mechanisms

Protein kinase C

Contact Info

Product

Resources

About

Loss of Ca²⁺‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca²⁺‐activated K⁺ channel opener

Loss of Ca²⁺‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca²⁺‐activated K⁺ channel opener

Aldosterone Regulation of Protein Kinase Signaling Pathways and Renal Na⁺Transport by Non-genomic Mechanisms