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 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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Acetylcholine / pharmacology
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Animals
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Arteries / drug effects
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Arteries / physiology*
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Calcium / metabolism*
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Calcium Channels, T-Type / genetics
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Calcium Channels, T-Type / physiology*
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Coronary Vessels / drug effects
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Coronary Vessels / pathology
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Coronary Vessels / physiology*
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Echocardiography
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Electrocardiography
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / physiology
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Female
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Fibrosis
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Ganglia, Spinal / cytology
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Gene Targeting
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Heart / physiology
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Heart Rate
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Muscle, Smooth, Vascular / physiology
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Myocardium / pathology
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Neurons / metabolism
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Nickel / pharmacology
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Nitric Oxide / physiology
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Nitric Oxide Donors / pharmacology
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Nitroprusside / pharmacology
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Patch-Clamp Techniques
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Vasoconstriction / drug effects
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Vasodilation* / drug effects
Substances
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Calcium Channels, T-Type
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Nitric Oxide Donors
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Nitroprusside
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Nitric Oxide
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Nickel
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Acetylcholine
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Calcium