Role of vascular potassium channels in the regulation of renal hemodynamics

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Standard

Role of vascular potassium channels in the regulation of renal hemodynamics. / Sørensen, Charlotte Mehlin; Braunstein, Thomas Hartig; von Holstein-Rathlou, Niels-Henrik; Salomonsson, Max.

I: American Journal of Physiology: Renal Physiology, Bind 302, Nr. 5, 01.03.2012, s. F505-F518.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Sørensen, CM, Braunstein, TH, von Holstein-Rathlou, N-H & Salomonsson, M 2012, 'Role of vascular potassium channels in the regulation of renal hemodynamics', American Journal of Physiology: Renal Physiology, bind 302, nr. 5, s. F505-F518. https://doi.org/10.1152/ajprenal.00052.2011

APA

Sørensen, C. M., Braunstein, T. H., von Holstein-Rathlou, N-H., & Salomonsson, M. (2012). Role of vascular potassium channels in the regulation of renal hemodynamics. American Journal of Physiology: Renal Physiology, 302(5), F505-F518. https://doi.org/10.1152/ajprenal.00052.2011

Vancouver

Sørensen CM, Braunstein TH, von Holstein-Rathlou N-H, Salomonsson M. Role of vascular potassium channels in the regulation of renal hemodynamics. American Journal of Physiology: Renal Physiology. 2012 mar. 1;302(5):F505-F518. https://doi.org/10.1152/ajprenal.00052.2011

Author

Sørensen, Charlotte Mehlin ; Braunstein, Thomas Hartig ; von Holstein-Rathlou, Niels-Henrik ; Salomonsson, Max. / Role of vascular potassium channels in the regulation of renal hemodynamics. I: American Journal of Physiology: Renal Physiology. 2012 ; Bind 302, Nr. 5. s. F505-F518.

Bibtex

@article{ffa234762bad4f29aea59063e6101289,
title = "Role of vascular potassium channels in the regulation of renal hemodynamics",
abstract = "K+ conductance is a major determinant of membrane potential (Vm) in vascular smooth muscle (VSMC) and endothelial cells (EC). The vascular tone is controlled by Vm through the action of voltage-operated Ca2+ channels (VOCC) in VSMC. Increased K+ conductance leads to hyperpolarization and vasodilation, while inactivation of K+ channels causes depolarization and vasoconstriction. K+ channels in EC indirectly participate in the control of vascular tone by several mechanisms, e.g., release of nitric oxide and endothelium-derived hyperpolarizing factor. In the kidney, a change in the activity of one or more classes of K+ channels will lead to a change in hemodynamic resistance and therefore of renal blood flow and glomerular filtration pressure. Through these effects, the activity of renal vascular K+ channels influences renal salt and water excretion, fluid homeostasis, and ultimately blood pressure. Four main classes of K+ channels [calcium activated (KCa), inward rectifier (Kir), voltage activated (KV), and ATP sensitive (KATP)] are found in the renal vasculature. Several in vitro experiments have suggested a role for individual classes of K+ channels in the regulation of renal vascular function. Results from in vivo experiments are sparse. We discuss the role of the different classes of renal vascular K+ channels and their possible role in the integrated function of the renal microvasculature. Since several pathological conditions, among them hypertension, are associated with alterations in K+ channel function, the role of renal vascular K+ channels in the control of salt and water excretion deserves attention. ",
author = "S{\o}rensen, {Charlotte Mehlin} and Braunstein, {Thomas Hartig} and {von Holstein-Rathlou}, Niels-Henrik and Max Salomonsson",
year = "2012",
month = mar,
day = "1",
doi = "10.1152/ajprenal.00052.2011",
language = "English",
volume = "302",
pages = "F505--F518",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "5",

}

RIS

TY - JOUR

T1 - Role of vascular potassium channels in the regulation of renal hemodynamics

AU - Sørensen, Charlotte Mehlin

AU - Braunstein, Thomas Hartig

AU - von Holstein-Rathlou, Niels-Henrik

AU - Salomonsson, Max

PY - 2012/3/1

Y1 - 2012/3/1

N2 - K+ conductance is a major determinant of membrane potential (Vm) in vascular smooth muscle (VSMC) and endothelial cells (EC). The vascular tone is controlled by Vm through the action of voltage-operated Ca2+ channels (VOCC) in VSMC. Increased K+ conductance leads to hyperpolarization and vasodilation, while inactivation of K+ channels causes depolarization and vasoconstriction. K+ channels in EC indirectly participate in the control of vascular tone by several mechanisms, e.g., release of nitric oxide and endothelium-derived hyperpolarizing factor. In the kidney, a change in the activity of one or more classes of K+ channels will lead to a change in hemodynamic resistance and therefore of renal blood flow and glomerular filtration pressure. Through these effects, the activity of renal vascular K+ channels influences renal salt and water excretion, fluid homeostasis, and ultimately blood pressure. Four main classes of K+ channels [calcium activated (KCa), inward rectifier (Kir), voltage activated (KV), and ATP sensitive (KATP)] are found in the renal vasculature. Several in vitro experiments have suggested a role for individual classes of K+ channels in the regulation of renal vascular function. Results from in vivo experiments are sparse. We discuss the role of the different classes of renal vascular K+ channels and their possible role in the integrated function of the renal microvasculature. Since several pathological conditions, among them hypertension, are associated with alterations in K+ channel function, the role of renal vascular K+ channels in the control of salt and water excretion deserves attention.

AB - K+ conductance is a major determinant of membrane potential (Vm) in vascular smooth muscle (VSMC) and endothelial cells (EC). The vascular tone is controlled by Vm through the action of voltage-operated Ca2+ channels (VOCC) in VSMC. Increased K+ conductance leads to hyperpolarization and vasodilation, while inactivation of K+ channels causes depolarization and vasoconstriction. K+ channels in EC indirectly participate in the control of vascular tone by several mechanisms, e.g., release of nitric oxide and endothelium-derived hyperpolarizing factor. In the kidney, a change in the activity of one or more classes of K+ channels will lead to a change in hemodynamic resistance and therefore of renal blood flow and glomerular filtration pressure. Through these effects, the activity of renal vascular K+ channels influences renal salt and water excretion, fluid homeostasis, and ultimately blood pressure. Four main classes of K+ channels [calcium activated (KCa), inward rectifier (Kir), voltage activated (KV), and ATP sensitive (KATP)] are found in the renal vasculature. Several in vitro experiments have suggested a role for individual classes of K+ channels in the regulation of renal vascular function. Results from in vivo experiments are sparse. We discuss the role of the different classes of renal vascular K+ channels and their possible role in the integrated function of the renal microvasculature. Since several pathological conditions, among them hypertension, are associated with alterations in K+ channel function, the role of renal vascular K+ channels in the control of salt and water excretion deserves attention.

U2 - 10.1152/ajprenal.00052.2011

DO - 10.1152/ajprenal.00052.2011

M3 - Journal article

VL - 302

SP - F505-F518

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 5

ER -

ID: 38256443