Abnormal coronary function in mice deficient in alpha1H T-type Ca2+ channels.
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.
Pubmed ID: 14631046 RIS Download
Acetylcholine | Animals | Arteries | Calcium | Calcium Channels, T-Type | Coronary Vessels | Echocardiography | Electrocardiography | Endothelium, Vascular | Female | Fibrosis | Ganglia, Spinal | Gene Targeting | Heart | Heart Rate | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Muscle, Smooth, Vascular | Myocardium | Neurons | Nickel | Nitric Oxide | Nitric Oxide Donors | Nitroprusside | Patch-Clamp Techniques | Vasoconstriction | Vasodilation