Distal potassium handling based on flow modulation of maxi-K channel activity

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

PURPOSE OF REVIEW: Studies on the mechanisms of distal K secretion have highlighted the importance of the renal outer-medullary K (ROMK) and maxi-K channels. This review considers several human disorders characterized by hypokalemia and hyperkalemia, as well as mouse models of these disorders, and the mechanisms by which ROMK and maxi-K may be dysregulated. RECENT FINDINGS: Analysis of knockout mice lacking ROMK, a model for type II Bartter's syndrome, has shown a role for maxi-K in distal K secretion. Knockout mice lacking either the α or β1 subunits of maxi-K also show deficits in flow-dependent K secretion. Analysis of transgenic and knock-in mouse models of pseudohypoaldosteronism type II, in which mutant forms of with-no-lysine kinase 4 are expressed, suggests ways in which ROMK and maxi-K may be dysregulated to result in hyperkalemia. Modeling studies also provide insights into the role of Na delivery vs. flow in K secretion. SUMMARY: The importance of both ROMK and maxi-K to distal K secretion is now well established, but the relative role that each of these two channels plays in normal and diseased states has not been definitively established. Analysis of human and animal model data can generate hypotheses for future experiments.

Original languageEnglish (US)
Pages (from-to)350-355
Number of pages6
JournalCurrent Opinion in Nephrology and Hypertension
Volume18
Issue number4
DOIs
StatePublished - Jul 2009

Fingerprint

Large-Conductance Calcium-Activated Potassium Channels
Potassium
Kidney
Hyperkalemia
Knockout Mice
Pseudohypoaldosteronism
Bartter Syndrome
Hypokalemia
Lysine
Phosphotransferases
Animal Models

Keywords

  • Bartter's syndrome
  • Ca-activated K channel
  • distal K secretion
  • diuretics
  • hyperkalemia
  • hypokalemia
  • maxi-K
  • pseudohypoaldosteronism type II
  • rat outer medullary K channel

ASJC Scopus subject areas

  • Nephrology
  • Internal Medicine

Cite this

@article{b073630ad2e64ea0b0a6befe77085bc1,
title = "Distal potassium handling based on flow modulation of maxi-K channel activity",
abstract = "PURPOSE OF REVIEW: Studies on the mechanisms of distal K secretion have highlighted the importance of the renal outer-medullary K (ROMK) and maxi-K channels. This review considers several human disorders characterized by hypokalemia and hyperkalemia, as well as mouse models of these disorders, and the mechanisms by which ROMK and maxi-K may be dysregulated. RECENT FINDINGS: Analysis of knockout mice lacking ROMK, a model for type II Bartter's syndrome, has shown a role for maxi-K in distal K secretion. Knockout mice lacking either the α or β1 subunits of maxi-K also show deficits in flow-dependent K secretion. Analysis of transgenic and knock-in mouse models of pseudohypoaldosteronism type II, in which mutant forms of with-no-lysine kinase 4 are expressed, suggests ways in which ROMK and maxi-K may be dysregulated to result in hyperkalemia. Modeling studies also provide insights into the role of Na delivery vs. flow in K secretion. SUMMARY: The importance of both ROMK and maxi-K to distal K secretion is now well established, but the relative role that each of these two channels plays in normal and diseased states has not been definitively established. Analysis of human and animal model data can generate hypotheses for future experiments.",
keywords = "Bartter's syndrome, Ca-activated K channel, distal K secretion, diuretics, hyperkalemia, hypokalemia, maxi-K, pseudohypoaldosteronism type II, rat outer medullary K channel",
author = "Rodan, {Aylin R.} and Huang, {Chou Long}",
year = "2009",
month = "7",
doi = "10.1097/MNH.0b013e32832c75d8",
language = "English (US)",
volume = "18",
pages = "350--355",
journal = "Current Opinion in Nephrology and Hypertension",
issn = "1062-4821",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Distal potassium handling based on flow modulation of maxi-K channel activity

AU - Rodan, Aylin R.

AU - Huang, Chou Long

PY - 2009/7

Y1 - 2009/7

N2 - PURPOSE OF REVIEW: Studies on the mechanisms of distal K secretion have highlighted the importance of the renal outer-medullary K (ROMK) and maxi-K channels. This review considers several human disorders characterized by hypokalemia and hyperkalemia, as well as mouse models of these disorders, and the mechanisms by which ROMK and maxi-K may be dysregulated. RECENT FINDINGS: Analysis of knockout mice lacking ROMK, a model for type II Bartter's syndrome, has shown a role for maxi-K in distal K secretion. Knockout mice lacking either the α or β1 subunits of maxi-K also show deficits in flow-dependent K secretion. Analysis of transgenic and knock-in mouse models of pseudohypoaldosteronism type II, in which mutant forms of with-no-lysine kinase 4 are expressed, suggests ways in which ROMK and maxi-K may be dysregulated to result in hyperkalemia. Modeling studies also provide insights into the role of Na delivery vs. flow in K secretion. SUMMARY: The importance of both ROMK and maxi-K to distal K secretion is now well established, but the relative role that each of these two channels plays in normal and diseased states has not been definitively established. Analysis of human and animal model data can generate hypotheses for future experiments.

AB - PURPOSE OF REVIEW: Studies on the mechanisms of distal K secretion have highlighted the importance of the renal outer-medullary K (ROMK) and maxi-K channels. This review considers several human disorders characterized by hypokalemia and hyperkalemia, as well as mouse models of these disorders, and the mechanisms by which ROMK and maxi-K may be dysregulated. RECENT FINDINGS: Analysis of knockout mice lacking ROMK, a model for type II Bartter's syndrome, has shown a role for maxi-K in distal K secretion. Knockout mice lacking either the α or β1 subunits of maxi-K also show deficits in flow-dependent K secretion. Analysis of transgenic and knock-in mouse models of pseudohypoaldosteronism type II, in which mutant forms of with-no-lysine kinase 4 are expressed, suggests ways in which ROMK and maxi-K may be dysregulated to result in hyperkalemia. Modeling studies also provide insights into the role of Na delivery vs. flow in K secretion. SUMMARY: The importance of both ROMK and maxi-K to distal K secretion is now well established, but the relative role that each of these two channels plays in normal and diseased states has not been definitively established. Analysis of human and animal model data can generate hypotheses for future experiments.

KW - Bartter's syndrome

KW - Ca-activated K channel

KW - distal K secretion

KW - diuretics

KW - hyperkalemia

KW - hypokalemia

KW - maxi-K

KW - pseudohypoaldosteronism type II

KW - rat outer medullary K channel

UR - http://www.scopus.com/inward/record.url?scp=67849096869&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67849096869&partnerID=8YFLogxK

U2 - 10.1097/MNH.0b013e32832c75d8

DO - 10.1097/MNH.0b013e32832c75d8

M3 - Article

VL - 18

SP - 350

EP - 355

JO - Current Opinion in Nephrology and Hypertension

JF - Current Opinion in Nephrology and Hypertension

SN - 1062-4821

IS - 4

ER -