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

Chien Chang Chen, Kathryn G. Lamping, Daniel W. Nuno, Rita Barresi, Sally J. Prouty, Julie L. Lavoie, Leanne L. Cribbs, Sarah K. England, Curt D. Sigmund, Robert M. Weiss, Roger A. Williamson, Joseph A. Hill, Kevin P. Campbell

Research output: Contribution to journalArticlepeer-review

306 Scopus citations


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.

Original languageEnglish
Pages (from-to)1416-1418
Number of pages3
Issue number5649
StatePublished - Nov 21 2003


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