Enhanced β-adrenergic response in mice with dominant-negative expression of the PKD2L1 channel

Manabu Murakami, Agnieszka M. Murakami, Takayuki Nemoto, Takayoshi Ohba, Manabu Yonekura, Yuichi Toyama, Hirofumi Tomita, Yasushi Matsuzaki, Daisuke Sawamura, Kazuyoshi Hirota, Shirou Itagaki, Yujiro Asada, Ichiro Miyoshi

Research output: Contribution to journalArticlepeer-review


Polycystic kidney disease (PKD) is the most common genetic cause of kidney failure in humans. Among the various PKD-related molecules, PKD2L1 forms cation channels, but its physiological importance is obscure. In the present study, we established a transgenic mouse line by overexpressing the dominant-negative form of the mouse PKD2L1 gene (i.e., lacking the pore-forming domain). The resulting PKD2L1del-Tg mice exhibited supraventricular premature contraction, as well as enhanced sensitivity to β-adrenergic stimulation and unstable R-R intervals in electrocardiography. During spontaneous atrial contraction, PKD2L1del-Tg atria showed enhanced sensitivity to isoproterenol, norepinephrine, and epinephrine. Action potential recording revealed a shortened action potential duration in PKD2L1del-Tg atria in response to isoproterenol. These findings indicated increased adrenergic sensitivity in PKD2L1del-Tg mice, suggesting that PKD2L1 is involved in sympathetic regulation.

Original languageEnglish
Article numbere0261668
JournalPloS one
Issue number1 January
Publication statusPublished - 2022 Jan

ASJC Scopus subject areas

  • General


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