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Na + /K + ‐pump modulates intercellular communication via interaction with other membrane transporters in vascular smooth muscle cells.
Author(s) -
Matchkov Vladimir V.,
Hansen Anne Kirstine,
Nilsson Holger,
Aalkjaer Christian
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a912-a
Subject(s) - ouabain , extracellular , vascular smooth muscle , biophysics , intracellular , chemistry , gap junction , membrane potential , sodium calcium exchanger , calcium , membrane , biochemistry , sodium , endocrinology , biology , smooth muscle , organic chemistry
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 + /Ca 2+ ‐exchanger in restricted spaces near the plasma membrane. The intracellular Ca 2+ concentration ([Ca 2+ ] 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 [Ca 2+ ] 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 K ATP channels. Inhibition of the Na + /Ca 2+ ‐exchange activity by SEA0400 or by lowering the extracellular Na + concentration also uncoupled the cells. Depletion of [Na + ] i and clamping low [Ca 2+ ] i prevented the uncoupling. The experiments suggest that the Na + /K + ‐pump may affect gap junction conductivity via localized changes in [Ca 2+ ] i through modulation of Na + /Ca 2+ ‐exchanger activity.