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Figure 3 Effect of seven days of PE infusion on (A) myocardial ß-adrenergic receptor (AR) responsiveness and (B) ßAR kinase 1 (ßARK1) levels in nontransgenic littermate control (NLC) hearts and the hearts of transgenic mice with cardiac targeted overexpression of the wild-type {alpha}1B-AR (Tg{alpha}43). (A) The activity of adenylyl cyclase from cardiac membranes was assessed basally and after isoproterenol (ISO) stimulation (10–4M). Data are expressed as the mean ± SEM of ISO-stimulated activity over the activity seen under basal conditions (n = 6 to 12). *p < 0.05 versus sham (phosphate-buffered saline) treatment; #p < 0.05 versus PE-treated NLC mice. (B) Myocardial levels of ßARK1 as measured by semiquantitative Western blotting following immunoprecipitation of cardiac extracts with a monoclonal ßARK1/2 antibody (16). Shown is the mean ± SEM of sham-treated NLC (n = 7) and Tg{alpha}43 (n = 11) mice compared with PE-treated (7 days) NLC (n = 6) and Tg{alpha}43 (n = 10) mice. ßARK1 levels in all mice were normalized to the levels found in sham (phosphate-buffered saline) NLC mice. Shown in the inset is a representative immunoblot of ßARK1 levels. *p < 0.05 versus sham-treated mice; #p < 0.05 versus NLC mice.





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