Abnormal Coronary Function in Mice Deficient in α1H T-type Ca2+ Channels

Abstract

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 α1H T-type Ca2+ channel (α13.2-null have constitutively constricted coronary arterioles and focal myocardial fibrosis. Coronary arteries isolated from α13.2-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 α 1H T-type Ca2+ channels is essential for normal relaxation of coronary arteries.