Ryo Yoshimoto1, Masatoshi Hori1, Katsuhito Takahashi2,3,4,
Shun-ichiro Taniguchi5, Motoya Katsuki6,
Hiroshi Ozaki1 and Hideaki Karaki1,*
1Department of Veterinary Pharmacology, Graduate School of
Agriculture and Life Sciences, The University of Tokyo, Tokyo 113-8511,
Japan
2Department of Medicine, Osaka Medical Center for Cancer and
Cardiovascular Diseases, Osaka 537-8511, Japan
3The Graduate School of Pharmaceutical Science, Osaka University,
Osaka 565-0871, Japan
4PRESTO, Japan Science and Technology Corporation
5Research Center on Aging and Adaptation, Shinshu University
School of Medicine, Nagano 657-0013, Japan
6Department of DNA Biology and Embryo Engineering, Institute
for Medical Science, The University of Tokyo, Tokyo 108-8639, Japan
*Corresponding author.ÊÊFax:+81-3-5841-8183
E-mail: ahkrki@mail.ecc.u-tokyo.ac.jp
Abstract: Role of h1 calponin on Ca2+-sensitivity of smooth
muscle contraction was investigated using h1 calponin gene-deficient mice
(CP-/-) and wild type mice (CP+/+). PGF2a
induced a comparable force in intact aorta of CP+/+ and CP-/-. DPB showed
similar effects to PGF2a.
In membrane-permeabilized ileal smooth muscle, PDBu enhanced Ca2+-sensitivity
of contraction comparably in CP+/+ and CP-/-. GTPg-S
showed similar effects. Our results suggest that h1 calponin does not regulate
Ca2+-sensitivity in the contractile mechanism of smooth muscle.
Keywords: Calponin, Ca2+-sensitization, Smooth muscle contraction
Copyright© The Japanese Pharmacological Society 2000
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