Modulation of membrane potential by an acetylcholine-activated potassium current in trout atrial myocytes
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Modulation of membrane potential by an acetylcholine-activated potassium current in trout atrial myocytes. / Molina, Cristina E; Gesser, Hans; Llach, Anna; Tort, Lluis; Hove-Madsen, Leif.
In: AM J PHYSIOL-REG I, Vol. 292, No. 1, 01.2007, p. R388-95.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Modulation of membrane potential by an acetylcholine-activated potassium current in trout atrial myocytes
AU - Molina, Cristina E
AU - Gesser, Hans
AU - Llach, Anna
AU - Tort, Lluis
AU - Hove-Madsen, Leif
PY - 2007/1
Y1 - 2007/1
N2 - 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 EC(50) 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.
AB - 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 EC(50) 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.
KW - Acetylcholine
KW - Action Potentials
KW - Animals
KW - Atropine
KW - Cell Separation
KW - Heart Atria
KW - Heart Ventricles
KW - In Vitro Techniques
KW - Membrane Potentials
KW - Microelectrodes
KW - Muscarinic Antagonists
KW - Myocytes, Cardiac
KW - Oncorhynchus mykiss
KW - Patch-Clamp Techniques
KW - Potassium Channels
KW - Potassium Channels, Inwardly Rectifying
KW - Ventricular Function
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1152/ajpregu.00499.2005
DO - 10.1152/ajpregu.00499.2005
M3 - SCORING: Journal article
C2 - 16959867
VL - 292
SP - R388-95
IS - 1
ER -