Background: The β-adrenergic augmentation of cardiac contraction, by increasing the conductivity of L-type voltage-gated Ca1.2 channels, is of great physiological and pathophysiological importance. Stimulation of β-adrenergic receptors (βAR) activates protein kinase A (PKA) through separation of regulatory (PKAR) from catalytic (PKAC) subunits.
View Article and Find Full Text PDFAndersen-Tawil syndrome (ATS) type-1 is associated with loss-of-function mutations in gene. encodes the tetrameric inward-rectifier potassium channel Kir2.1, important to the resting phase of the cardiac action potential.
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