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- Title
Preferential Expression of Ca 2+ -Stimulable Adenylyl Cyclase III in the Supraventricular Area, including Arrhythmogenic Pulmonary Vein of the Rat Heart.
- Authors
Okamoto, Yosuke; Aung, Naing Ye; Tanaka, Masahiro; Takeda, Yuji; Takagi, Daichi; Igarashi, Wataru; Ishii, Kuniaki; Yamakawa, Mitsunori; Ono, Kyoichi
- Abstract
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.
- Subjects
ADENYLATE cyclase; HEART; PULMONARY veins; ATRIAL fibrillation; SOLAR cells; RATS; WESTERN immunoblotting
- Publication
Biomolecules (2218-273X), 2022, Vol 12, Issue 5, p724
- ISSN
2218-273X
- Publication type
Article
- DOI
10.3390/biom12050724