Vladimir Matchkov

Na+/K+-pump modulates intercellular communication viainteraction with other membrane transporters in vascularsmooth muscle cells.

Research output: Contribution to conferenceConference abstract for conferenceResearch

Standard

Na+/K+-pump modulates intercellular communication viainteraction with other membrane transporters in vascularsmooth muscle cells. / Matchkov, Vladimir; Hansen, Anne Kirstine; Nilsson, Holger et al.

2007. Abstract from Experimental Biology 2007, Washington, United States.

Research output: Contribution to conferenceConference abstract for conferenceResearch

Harvard

Matchkov, V, Hansen, AK, Nilsson, H & Aalkjær, C 2007, 'Na+/K+-pump modulates intercellular communication viainteraction with other membrane transporters in vascularsmooth muscle cells.', Experimental Biology 2007, Washington, United States, 27/04/2007 - 02/05/2007.

APA

Matchkov, V., Hansen, A. K., Nilsson, H., & Aalkjær, C. (2007). Na+/K+-pump modulates intercellular communication viainteraction with other membrane transporters in vascularsmooth muscle cells.. Abstract from Experimental Biology 2007, Washington, United States.

CBE

MLA

Matchkov, Vladimir et al. Na+/K+-pump modulates intercellular communication viainteraction with other membrane transporters in vascularsmooth muscle cells.. Experimental Biology 2007, 27 Apr 2007, Washington, United States, Conference abstract for conference, 2007. 1 p.

Vancouver

Author

Matchkov, Vladimir ; Hansen, Anne Kirstine ; Nilsson, Holger et al. / Na+/K+-pump modulates intercellular communication viainteraction with other membrane transporters in vascularsmooth muscle cells. Abstract from Experimental Biology 2007, Washington, United States.1 p.

Bibtex

@conference{f15ced801d8411dcbee902004c4f4f50,
title = "Na+/K+-pump modulates intercellular communication viainteraction with other membrane transporters in vascularsmooth muscle cells.",
abstract = "Ouabain, an inhibitor of the Na+/K+-pump, has previously been shown to disturb intercellular communication. Here we test the hypothesis that the communication between vascular smooth muscle cells (SMCs) is regulated through an interaction between the Na+/K+-pump and the Na+/Ca2+-exchanger in restricted spaces near the plasma membrane.The intracellular Ca2+ concentration ([Ca2+]i) in individual SMCs was imaged simultaneously with isometric force in rat mesenteric small arteries. Paired cultured rat aortic smooth muscle cells (A7r5) were used as a model for electrical coupling of SMC by measuring membrane capacitance (Cm).SMCs were uncoupled (evaluated by inhibition of vasomotion and desynchronization of [Ca2+]i transients in vascular wall, or by reduction of Cm measured in electrically coupled A7r5 cells) when the Na+/K+-pump was inhibited either by a low concentration of ouabain (1-10 µM) or by ATP depletion. Reduction of Na+/K+-pump activity by removal of extracellular K+ also uncoupled cells, but only after inhibition of KATP channels. Inhibition of the Na+/Ca2+-exchange activity by SEA0400 or by lowering the extracellular Na+ concentration also uncoupled the cells. Depletion of [Na+]i and clamping low [Ca2+]i prevented the uncoupling.The experiments suggest that the Na+/K+-pump may affect gap junction conductivity via localized changes in [Ca2+]i through modulation of Na+/Ca2+-exchanger activity.",
author = "Vladimir Matchkov and Hansen, {Anne Kirstine} and Holger Nilsson and Christian Aalkj{\ae}r",
year = "2007",
language = "English",
note = "null ; Conference date: 27-04-2007 Through 02-05-2007",

}

RIS

TY - ABST

T1 - Na+/K+-pump modulates intercellular communication viainteraction with other membrane transporters in vascularsmooth muscle cells.

AU - Matchkov, Vladimir

AU - Hansen, Anne Kirstine

AU - Nilsson, Holger

AU - Aalkjær, Christian

PY - 2007

Y1 - 2007

N2 - Ouabain, an inhibitor of the Na+/K+-pump, has previously been shown to disturb intercellular communication. Here we test the hypothesis that the communication between vascular smooth muscle cells (SMCs) is regulated through an interaction between the Na+/K+-pump and the Na+/Ca2+-exchanger in restricted spaces near the plasma membrane.The intracellular Ca2+ concentration ([Ca2+]i) in individual SMCs was imaged simultaneously with isometric force in rat mesenteric small arteries. Paired cultured rat aortic smooth muscle cells (A7r5) were used as a model for electrical coupling of SMC by measuring membrane capacitance (Cm).SMCs were uncoupled (evaluated by inhibition of vasomotion and desynchronization of [Ca2+]i transients in vascular wall, or by reduction of Cm measured in electrically coupled A7r5 cells) when the Na+/K+-pump was inhibited either by a low concentration of ouabain (1-10 µM) or by ATP depletion. Reduction of Na+/K+-pump activity by removal of extracellular K+ also uncoupled cells, but only after inhibition of KATP channels. Inhibition of the Na+/Ca2+-exchange activity by SEA0400 or by lowering the extracellular Na+ concentration also uncoupled the cells. Depletion of [Na+]i and clamping low [Ca2+]i prevented the uncoupling.The experiments suggest that the Na+/K+-pump may affect gap junction conductivity via localized changes in [Ca2+]i through modulation of Na+/Ca2+-exchanger activity.

AB - Ouabain, an inhibitor of the Na+/K+-pump, has previously been shown to disturb intercellular communication. Here we test the hypothesis that the communication between vascular smooth muscle cells (SMCs) is regulated through an interaction between the Na+/K+-pump and the Na+/Ca2+-exchanger in restricted spaces near the plasma membrane.The intracellular Ca2+ concentration ([Ca2+]i) in individual SMCs was imaged simultaneously with isometric force in rat mesenteric small arteries. Paired cultured rat aortic smooth muscle cells (A7r5) were used as a model for electrical coupling of SMC by measuring membrane capacitance (Cm).SMCs were uncoupled (evaluated by inhibition of vasomotion and desynchronization of [Ca2+]i transients in vascular wall, or by reduction of Cm measured in electrically coupled A7r5 cells) when the Na+/K+-pump was inhibited either by a low concentration of ouabain (1-10 µM) or by ATP depletion. Reduction of Na+/K+-pump activity by removal of extracellular K+ also uncoupled cells, but only after inhibition of KATP channels. Inhibition of the Na+/Ca2+-exchange activity by SEA0400 or by lowering the extracellular Na+ concentration also uncoupled the cells. Depletion of [Na+]i and clamping low [Ca2+]i prevented the uncoupling.The experiments suggest that the Na+/K+-pump may affect gap junction conductivity via localized changes in [Ca2+]i through modulation of Na+/Ca2+-exchanger activity.

M3 - Conference abstract for conference

Y2 - 27 April 2007 through 2 May 2007

ER -