| First Author | Murakami M | Year | 2022 |
| Journal | PLoS One | Volume | 17 |
| Issue | 1 | Pages | e0261668 |
| PubMed ID | 35051185 | Mgi Jnum | J:321293 |
| Mgi Id | MGI:6857247 | Doi | 10.1371/journal.pone.0261668 |
| Citation | Murakami M, et al. (2022) Enhanced beta-adrenergic response in mice with dominant-negative expression of the PKD2L1 channel. PLoS One 17(1):e0261668 |
| abstractText | 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 beta-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. |
