| First Author | Chen CC | Year | 2003 |
| Journal | Science | Volume | 302 |
| Issue | 5649 | Pages | 1416-8 |
| PubMed ID | 14631046 | Mgi Jnum | J:86616 |
| Mgi Id | MGI:2680867 | Doi | 10.1126/science.1089268 |
| Citation | Chen CC, et al. (2003) Abnormal coronary function in mice deficient in alpha1H T-type Ca2+ channels. Science 302(5649):1416-8 |
| abstractText | Calcium ion (Ca2+) influx through voltage-gated Ca2+ channels is important for the regulation of vascular tone. Activation of L-type Ca2+ channels initiates muscle contraction; however, the role of T-type Ca2+ channels (T-channels) is not clear. We show that mice deficient in the alpha1H T-type Ca2+ channel (alpha(1)3.2-null) have constitutively constricted coronary arterioles and focal myocardial fibrosis. Coronary arteries isolated from alpha(1)3.2-null arteries showed normal contractile responses, but reduced relaxation in response to acetylcholine and nitroprusside. Furthermore, acute blockade of T-channels with Ni2+ prevented relaxation of wild-type coronary arteries. Thus, Ca2+ influx through alpha1H T-type Ca2+ channels is essential for normal relaxation of coronary arteries. |
