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Article

Preferential Expression of Ca2+-Stimulable Adenylyl Cyclase III in the Supraventricular Area, including Arrhythmogenic Pulmonary Vein of the Rat Heart

1
Department of Cell Physiology, Akita Graduate School of Medicine, Hondo 010-8543, Japan
2
Pathological and Image Analysis Center, Cancer Research Center, Faculty of Medicine, Yamagata University, Iida-Nishi 990-9585, Japan
3
Department of Pharmacology, Faculty of Medicine, Yamagata University, Iida-Nishi 990-9585, Japan
4
Department of Immunology, Faculty of Medicine, Yamagata University, Iida-Nishi 990-9585, Japan
5
Department of Cardiovascular Surgery, Akita Graduate School of Medicine, Hondo 010-8543, Japan
*
Authors to whom correspondence should be addressed.
Academic Editor: Pietro Scicchitano
Biomolecules 2022, 12(5), 724; https://doi.org/10.3390/biom12050724
Received: 5 April 2022 / Revised: 16 May 2022 / Accepted: 19 May 2022 / Published: 20 May 2022
(This article belongs to the Special Issue Molecular Pathogenesis of Cardiac Arrhythmia)
Ectopic excitability in pulmonary veins (PVs) is the major cause of atrial fibrillation. We previously reported that the inositol trisphosphate receptor in rat PV cardiomyocytes cooperates with the Na+-Ca2+ exchanger to provoke ectopic automaticity in response to norepinephrine. Here, we focused on adenylyl cyclase (AC) as another effector of norepinephrine stimulation. RT-PCR, immunohistochemistry, and Western blotting revealed that the abundant expression of Ca2+-stimulable AC3 was restricted to the supraventricular area, including the PVs. All the other AC isotypes hardly displayed any region-specific expressions. Immunostaining of isolated cardiomyocytes showed an enriched expression of AC3 along the t-tubules in PV myocytes. The cAMP-dependent response of L-type Ca2+ currents in the PV and LA cells is strengthened by the 0.1 mM intracellular Ca2+ condition, unlike in the ventricular cells. The norepinephrine-induced automaticity of PV cardiomyocytes was reversibly suppressed by 100 µM SQ22536, an adenine-like AC inhibitor. These findings suggest that the specific expression of AC3 along t-tubules may contribute to arrhythmogenic automaticity in rat PV cardiomyocytes. View Full-Text
Keywords: adenylyl cyclase; supraventricular area; pulmonary vein; arrhythmia; atrial fibrillation; t-tubule adenylyl cyclase; supraventricular area; pulmonary vein; arrhythmia; atrial fibrillation; t-tubule
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MDPI and ACS Style

Okamoto, Y.; Aung, N.Y.; Tanaka, M.; Takeda, Y.; Takagi, D.; Igarashi, W.; Ishii, K.; Yamakawa, M.; Ono, K. Preferential Expression of Ca2+-Stimulable Adenylyl Cyclase III in the Supraventricular Area, including Arrhythmogenic Pulmonary Vein of the Rat Heart. Biomolecules 2022, 12, 724. https://doi.org/10.3390/biom12050724

AMA Style

Okamoto Y, Aung NY, Tanaka M, Takeda Y, Takagi D, Igarashi W, Ishii K, Yamakawa M, Ono K. Preferential Expression of Ca2+-Stimulable Adenylyl Cyclase III in the Supraventricular Area, including Arrhythmogenic Pulmonary Vein of the Rat Heart. Biomolecules. 2022; 12(5):724. https://doi.org/10.3390/biom12050724

Chicago/Turabian Style

Okamoto, Yosuke, Naing Ye Aung, Masahiro Tanaka, Yuji Takeda, Daichi Takagi, Wataru Igarashi, Kuniaki Ishii, Mitsunori Yamakawa, and Kyoichi Ono. 2022. "Preferential Expression of Ca2+-Stimulable Adenylyl Cyclase III in the Supraventricular Area, including Arrhythmogenic Pulmonary Vein of the Rat Heart" Biomolecules 12, no. 5: 724. https://doi.org/10.3390/biom12050724

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