In adult rat hearts in vivo, pressure overload-induced c-fos expression is mediated by beta-adrenergic stimulation rather than AT1 receptor activation, contrasting with findings in neonatal myocytes.
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Challenges neonatal myocyte data by implicating beta-adrenergic signaling in adult rat hypertrophy; hypothesis-generating for human pressure-overload therapies.
We determined the contributions of angiotensin II type 1 receptor (AT(1)) stimulation, adrenergic stimulation, and autonomic activation to pressure overload-induced c-fos expression in the adult rat heart in vivo. c-fos expression was increased in pressure-overloaded hearts created by aortic banding compared with sham-operated rats (458 +/- 100% vs. sham, P < 0.05). GR-138950, a selective AT(1) antagonist, did not blunt this expression (banding vs. banding + GR-138950: 458 +/- 100% vs. 500 +/- 125%, not significant). Atropine and hexamethonium partially decreased c-fos expression (banding vs. banding + atropine/hexamethonium: 700 +/- 67% vs. 400 +/- 67%, P < 0.05). Phentolamine had no significant effect on c-fos expression; however, propranolol inhibited the expression (banding vs. banding + propranolol: 492 +/- 108% vs. 154 +/- 15%, P < 0.05). The inhibition by propranolol was independent of the decreases in heart rate. Thus factors contributing to pressure overload-induced c-fos expression in adult rat hearts in vivo are different from those in neonatal myocytes in vitro undergoing stretch.
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Oginö et al. (1999) studied this question.
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