Subcellular mechanism for Ca(2+)-dependent enhancement of delayed rectifier K+ current in isolated membrane patches of guinea pig ventricular myocytes.
Population
Large-pipette inside-out membrane patches excised from isolated guinea pig ventricular myocytes
Comparison
Raising intracellular Ca2+ concentration from 10… vs Baseline [Ca2+]i (10 mol/L) and inactive…
Design
Preclinical
Authors
Discussion
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Implication
Physiological Ca2+ enhances cardiac IK via calmodulin; extends mechanistic insight but leaves open human relevance and arrhythmogenic effects.
Structured PICO
P
Population
Large-pipette inside-out membrane patches excised from isolated guinea pig ventricular myocytes
I
Intervention
Raising intracellular Ca2+ concentration ([Ca2+]i) from 10(-8) to 10(-6) mol/L, with and without calmodulin antagonists or protein kinase inhibitors
C
Comparator
Baseline [Ca2+]i (10(-8) mol/L) and inactive analogue W5
O
Outcome
Amplitude of delayed rectifier K+ current (IK) measured at +80 mVsurrogate
Cardiac delayed rectifier K+ current is enhanced by physiological increases in intracellular Ca2+ via a calmodulin-dependent pathway that does not involve phosphorylation.
Cite This Study
Nitta et al. (1994) studied this question.