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. 2002 Feb;135(3):581–588. doi: 10.1038/sj.bjp.0704495

Figure 3.

Figure 3

Peroxynitrite inhibited myofibrillar force development and in situ creatine kinase activity in vitro. Isolated cardiac trabeculae were infused with sub-micromolar concentrations of ONOO−, then ability to generate calcium-activated force and tyrosine nitration were assessed and tyrosine nitration. ATP solutions directly stimulate contractile activity; phosphocreatine (PCr) solutions require active MM-CK to elicit contraction. (A) Average fitted pCa/tension relationships for ATP and PCr solutions following ONOO− treatment. Control curves for ATP and PCr solutions were not statistically different, and were therefore pooled into one control treatment. (B) Fitted maximal force following ONNO− administration. Steady state ONOO− concentrations of 300 nM resulted in contractile deficits; ONOO− as low as 50 nM impaired MM-CK activity (PCr/ATP developed tension). (C) Representative western blot of M-CK probed for extent of tyrosine nitration with 3NT antibody. ONOO− caused concentration-dependent increases in 3NT immunoreactivity of M-CK (migration of M-CK confirmed with antibody against M-CK). *P<0.05 vs. control; †P<0.05 vs ATP at 50 nM ONOO−.