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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


  • Chen CC
  • Lamping KG
  • Nuno DW
  • Barresi R
  • Prouty SJ
  • Lavoie JL
  • Cribbs LL
  • England SK
  • Sigmund CD
  • Weiss RM
  • Williamson RA
  • Hill JA
  • Campbell KP


Science (New York, N.Y.)

Publication Data

November 21, 2003

Associated Grants


Mesh Terms

  • 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