Why the study?
Does bradykinin-stimulated nitric oxide release prevent angiotensin II-induced hypertrophy in adult rat cardiomyocytes?
Does bradykinin-stimulated nitric oxide release prevent angiotensin II-induced hypertrophy in adult rat cardiomyocytes?
Bradykinin prevents angiotensin II-induced cardiomyocyte hypertrophy in vitro through an endothelium-dependent nitric oxide pathway.
Supports NO-dependent antihypertrophic signaling in vitro; hypothesis-generating and requires in vivo validation before any clinical consideration.
The aim of the present study was to test the hypothesis that bradykinin-stimulated release of nitric oxide (NO) and/or prostacyclin from endothelium blocks myocyte hypertrophy in vitro. Angiotensin II increased [3H]phenylalanine incorporation by 21 +/- 2% in myocytes cocultured with endothelial cells; this was abolished by bradykinin in the presence of endothelial cells. Bradykinin increased cytosolic concentrations of cGMP by 29 +/- 4% in myocytes cocultured with endothelial cells. This was abolished by inhibition of NO synthase and by a cyclooxygenase inhibitor. Angiotensin II also increased [3H]phenylalanine incorporation by 28 +/- 3% in myocytes cultured in the absence of endothelial cells. This effect of angiotensin II in monoculture was abolished by donors of NO but not by bradykinin. Neither the stable analog of prostacyclin (iloprost) nor the prostacyclin second messanger analog 8-bromo-cAMP (8-BrcAMP) blocked the effect of angiotensin II. Furthermore, 8-BrcAMP and iloprost individually increased [3H]phenylalanine incorporation. The antihypertrophic effects of bradykinin are critically dependent on endothelium-derived NO.
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Ritchie et al. (1998) studied this question.
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