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. Author manuscript; available in PMC: 2022 Mar 1.
Published in final edited form as: Pflugers Arch. 2021 Jan 7;473(3):491–506. doi: 10.1007/s00424-020-02500-3

Table 3.

The role of IKAS blockade on pulmonary vein and cardiac conduction systems

Region Model Agents Species Sex experimental settings Ca2+ (mmol/L)* K+ (mmol/L)* Effects of IKAS blockade on automaticity Effects of IKAS on MDP Effects of IKAS on AP amplitude Effects of IKAS blockade on APD Reference
PV Remodeled atria by 7-day atrial tachypacing NS8593 Dog NA In vivo, single cells Normal Normal NA No effect No effect Prolong APD [70]
PV Normal atria with intermittent burst pacing Apamin Rabbit Male Tissue, single cells 0.9 4.0 NA Prolong APD [68]
Non-denudated PV Normal atria Apamin Rabbit NA Tissue, single cells 2.7 4.0 Increase automaticity No effect No effect No effect [11]
Denudated PV Normal atria Apamin Rabbit NA Tissue, single cells 2.7 4.0 Decrease automaticity No effect No effect Prolong APD [11]
SA node Normal atria Apamin Rabbit NA Tissue, single cells 2.7 4.0 Decrease automaticity No effect No effect Prolong APD [11]
SA node atria Apamin Wildtype mouse Female, male Tissue, single cells 1.8 5.4 Decrease automaticity Decrease MDP NA Prolong APD [87]
SA node atria Apamin NCX knockout mouse Female, male Tissue, single cells 1.8 5.4 No effect on firing rate, but increase firing regularity NA NA Prolong APD [87]
Purkinje fiber Normal ventricle with AV block Apamin Rabbit Female, male Isolated heart and pseudotendon 1.8 4.0 Increase automaticity No effect on MDP, but lower the threshold potential for phase 0 depolarization No effect Prolong APD [72,93]

AV, atrioventricular block; APD, action potential duration; PV, pulmonary vein; MDP, maximal diastolic potential; NCX, sodium-calcium exchanger; SA, sinoatrial