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This Article Full Text Full Text (PDF) All Versions of this Article: 292/1/R388    most recent 00499.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Molina, C. E. Articles by Hove-Madsen, L. Search for Related Content PubMed PubMed Citation Articles by Molina, C. E. Articles by Hove-Madsen, L.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Modulation of membrane potential by an acetylcholine-activated potassium current in trout atrial myocytes

¹Cardiology Department, Institut Català de Cienciès Cardiovasculars, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; ²Department of Zoophysiology, Biological Institute, University of Århus, Universitetsparken, Århus C, Denmark; and ³Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain

Submitted 8 July 2005 ; accepted in final form 1 September 2006

Application of the current-clamp technique in rainbow trout atrial myocytes has yielded resting membrane potentials that are incompatible with normal atrial function. To investigate this paradox, we recorded the whole membrane current (I_m) and compared membrane potentials recorded in isolated cardiac myocytes and multicellular preparations. Atrial tissue and ventricular myocytes had stable resting potentials of –87 ± 2 mV and –83.9 ± 0.4 mV, respectively. In contrast, 50 out of 59 atrial myocytes had unstable depolarized membrane potentials that were sensitive to the holding current. We hypothesized that this is at least partly due to a small slope conductance of I_m around the resting membrane potential in atrial myocytes. In accordance with this hypothesis, the slope conductance of I_m was about sevenfold smaller in atrial than in ventricular myocytes. Interestingly, ACh increased I_m at –120 mV from 4.3 pA/pF to 27 pA/pF with an EC₅₀ of 45 nM in atrial myocytes. Moreover, 3 nM ACh increased the slope conductance of I_m fourfold, shifted its reversal potential from –78 ± 3 to –84 ± 3 mV, and stabilized the resting membrane potential at –92 ± 4 mV. ACh also shortened the action potential in both atrial myocytes and tissue, and this effect was antagonized by atropine. When applied alone, atropine prolonged the action potential in atrial tissue but had no effect on membrane potential, action potential, or I_m in isolated atrial myocytes. This suggests that ACh-mediated activation of an inwardly rectifying K⁺ current can modulate the membrane potential in the trout atrial myocytes and stabilize the resting membrane potential.

teleost heart; I_K,ACh; cholinergic modulation; action potential

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