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. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: Circ Arrhythm Electrophysiol. 2021 Sep 30;14(10):e010082. doi: 10.1161/CIRCEP.121.010082

Figure 7.

Figure 7.

Schematic showing the signal transduction cascade that mediates ventricular tachycardia due to cAMP-mediated triggered activity. Clinical right ventricular outflow tract tachycardia is usually adrenergically-mediated, and is frequently triggered by exercise or stress. In contrast, the somatic mutation W234R Gsα doesn’t require an agonist for activation since it is constitutively active, accounting for resting ventricular tachycardia. Abbreviations: AC, adenylyl cyclase; A1AR, adenosine receptor A1; ACH; acetylcholine; ADO, adenosine; β-AR, β-adrenergic receptor; CICR, calcium-induced calcium release; DAD, delayed afterdepolarization; Gi2α, inhibitory G-protein; Gsα, stimulatory G-protein; Iti, transient inward current; LTCC, L-type calcium channel; mAChR, muscarinic acetylcholine receptor; NCX, sodium–calcium exchanger; PKA, cAMP-dependent protein kinase (protein kinase A); PLB, phospholamban; RyR2, ryanodine receptor; SERCA, sarco/endoplamic reticulum Ca2+-ATPase; SR, sarcoplasmic reticulum.