January 1, 1998The Japanese Journal of PharmacologyOpen Access

Acetylcholine-Induced Biphasic Effect on the Maximum Upstroke Velocity of Action Potential in Mouse Right Atria: Interaction With β-Adrenergic Signaling Cascade

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Population

Isolated mouse right atria

Design

Preclinical

Authors

IAIslam Md. AmirulTohoku Medical and Pharmaceutical University HNHiroshi NojimaThe University of Osaka IKIkuko KimuraTokyo Medical University

Discussion

Member takes

Implication

Beta-adrenergic antagonism of muscarinic effects on atrial Vmax in mice leaves open relevance to human conduction or arrhythmias; hypothesis-generating.

Structured PICO

Population

Isolated mouse right atria

Intervention

Isoproterenol (3 nM) and other pharmacological modulators (propranolol, McN-A-343, oxotremorine, cholera toxin, forskolin, H-89)

Outcome

Maximum upstroke velocity of action potential (Vmax)surrogate

Activation of the beta-adrenergic-Gs-adenylyl cyclase system antagonizes muscarinic M1-mediated reduction and potentiates M2-mediated increase in action potential upstroke velocity in mouse atria.

Cite This Study

Amirul et al. (1998) studied this question.

synapsesocial.com/papers/6a7e4072fff18652e232f44a https://doi.org/10.1254/jjp.78.181

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Implication

Beta-adrenergic antagonism of muscarinic effects on atrial Vmax in mice leaves open relevance to human conduction or arrhythmias; hypothesis-generating.

Acetylcholine-Induced Biphasic Effect on the Maximum Upstroke Velocity of Action Potential in Mouse Right Atria: Interaction With β-Adrenergic Signaling Cascade

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Acetylcholine-Induced Biphasic Effect on the Maximum Upstroke Velocity of Action Potential in Mouse Right Atria: Interaction With β-Adrenergic Signaling Cascade

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider