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Am J Physiol Heart Circ Physiol (May 16, 2002). doi:10.1152/ajpheart.00232.2002
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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00232.2002
Submitted on March 18, 2002
Accepted on May 13, 2002

{alpha} 1 -AR induced positive inotropic response in the heart is dependent on myosin light chain phosphorylation

Geir O. Andersen1*, Eirik Qvigstad2, Iwona G. Schiander2, Halfdan Aass3, Jan-Bjorn Osnes2, and Tor Skomedal2

1 Department of Pharmacology, University of Oslo, Oslo, Norway; MSD Cardiovascular Research Center, Rikshospitalet University Hospital, Oslo, Norway
2 Department of Pharmacology, University of Oslo, Oslo, Norway
3 Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway

* To whom correspondence should be addressed. E-mail: g.o.andersen{at}labmed.uio.no.

The possible involvement of different kinases in the {alpha} 1 -AR mediated positive inotropic effect (PIE) was investigated in rat papillary muscle and compared to ß-AR, endothelin receptor and phorbol ester induced changes in contractility. The {alpha} 1 -AR induced PIE was not reduced by inhibitors of PKC, MAPK (ERK and p38), PI 3-kinase or CaMKII. PKC inhibition attenuated, however, the effect of the phorbol ester PMA on contractility. {alpha} 1 -AR induced PIE was reduced by about 90 % during inhibition of myosin light chain kinase (MLCK) by ML-9. Endothelin induced PIE was also reduced by ML-9, but ML-9 had no effect on ß-AR induced PIE. The Rho kinase inhibitor Y-27632 also reduced the {alpha} 1 -AR induced PIE. {alpha} 1 -AR induced PIE in muscle strips from explanted failing human hearts was also sensitive to myosin light chain kinase inhibition. {alpha} 1 -AR induced a modest increase in 32P incorporation into myosin light chain in isolated rat cardiomyocytes. This effect was eliminated by ML-9. The PIE of {alpha} 1 -AR stimulation seems to be dependent on myosin light chain phosphorylation.




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