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Am J Physiol Heart Circ Physiol 283: H1471-H1480, 2002. First published May 16, 2002; doi:10.1152/ajpheart.00232.2002
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Vol. 283, Issue 4, H1471-H1480, October 2002

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

Geir Øystein Andersen1,2,4, Eirik Qvigstad1, Iwona Schiander1, Halfdan Aass3, Jan-Bjørn Osnes1, and Tor Skomedal1

1 Department of Pharmacology, 2 Merck Sharp & Dohme Cardiovascular Research Center, and 3 Department of Cardiology, Rikshospitalet University Hospital, 4 Department of Internal Medicine, Ullerål University Hospital, University of Oslo, N-0316 Oslo, Norway

The possible involvement of different kinases in the alpha 1-adrenoreceptor (AR)-mediated positive inotropic effect (PIE) was investigated in rat papillary muscle and compared with beta -AR-, endothelin receptor- and phorbol ester-induced changes in contractility. The alpha 1-AR-induced PIE was not reduced by the inhibitors of protein kinase C (PKC), MAPK (ERK and p38), phosphatidyl inositol 3-kinase, or calmodulin kinase II. However, PKC inhibition attenuated the effect of phorbol 12-myristate 13-acetate (PMA) on contractility. alpha 1-AR-induced PIE was reduced by ~90% during inhibition of myosin light chain kinase (MLCK) by 1-(5-chloronaphthalene-1-sulfonyl)1H-hexahydro-1,4-diazepine (ML-9). Endothelin-induced PIE was also reduced by ML-9, but ML-9 had no effect on beta -AR-induced PIE. The Rho kinase inhibitor Y-27632 also reduced the alpha 1-AR-induced PIE. The alpha 1-AR-induced PIE in muscle strips from explanted failing human hearts was also sensitive to MLCK 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 MLCK phosphorylation.

endothelin; inhibitors; 1-(5-chloronaphthalene-1-sulfonyl)1H- hexahydro-1,4-diazepine; phenylephrine; Rho kinase; alpha -adrenoreceptor


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