| First Author | Zingman LV | Year | 2002 |
| Journal | Proc Natl Acad Sci U S A | Volume | 99 |
| Issue | 20 | Pages | 13278-83 |
| PubMed ID | 12271142 | Mgi Jnum | J:79518 |
| Mgi Id | MGI:2388431 | Doi | 10.1073/pnas.212315199 |
| Citation | Zingman LV, et al. (2002) Kir6.2 is required for adaptation to stress. Proc Natl Acad Sci U S A 99(20):13278-83 |
| abstractText | Reaction to stress requires feedback adaptation of cellular functions to secure a response without distress, but the molecular order of this process is only partially understood. Here, we report a previously unrecognized regulatory element in the general adaptation syndrome. Kir6.2, the ion-conducting subunit of the metabolically responsive ATP-sensitive potassium (K(ATP)) channel, was mandatory for optimal adaptation capacity under stress. Genetic deletion of Kir6.2 disrupted K(ATP) channel-dependent adjustment of membrane excitability and calcium handling, compromising the enhancement of cardiac performance driven by sympathetic stimulation, a key mediator of the adaptation response. In the absence of Kir6.2, vigorous sympathetic challenge caused arrhythmia and sudden death, preventable by calcium-channel blockade. Thus, this vital function identifies a physiological role for K(ATP) channels in the heart. |
