Antioxidant and antiinflammatory effect of carvedilol in mononuclear cells of hypertensive patients

Yasunary et al have recently reported that carvedilol treatment decreased oxidative stress and C-reactive protein level in mononuclear cells from essential hypertensive patients compared with propranolol, even though the decrease in mean arterial pressure was similar. Given the known relation between cardiovascular risk and oxidative stress, inflammation, and C-reactive protein, the authors suggested that carvedilol may have anti-inflammatory effects, possibly by decreasing oxidative stress in mononuclear cells. We would like to point out that we have provided further evidence of carvedilol’s antioxidant and antiinflammatory effect based on the results of our study examining carvedilol’s effect on cyclosporin-induced post-transplant hypertension. Hypertension is a common finding during treatment with calcineurin inhibitors such as cyclosporin and tacrolimus, as they are powerful stimulators of oxidative stress, which leads to hypertension and its long-term complication, such as cardiovascular remodeling and atherogenesis through nitric oxide degradation, endothelial dysfunction, and increased production of transforming growth factor β (TGFβ). We reported that carvedilol treatment decreased blood pressure and oxidative stress markers, such as plasma levels of nitrotyrosine, an extimate of peroxynitrite, and mononuclear cell TGFβ mRNA production. In addition, carvedilol treatment increased both plasma antioxidant power and mononuclear cell heme oxygenase-1 mRNA production in these patients. These changes are potentially important, as TGFβ is a major profibrotic cytokine and heme oxygenase-1 is protective against oxidative stress and possesses long-term anti-inflammatory and antiproliferative effects. ^,  Finally, the carvedilol-induced reduction of peroxynitrite level suggests that nitric oxide bioavailability increased.

In conclusion, the results of our study in mononuclear cells of post-transplant hypertensive patients, when combined with those reported by Yasunari et al, provide substantial evidence for the antioxidant and anti-inflammatory effects of carvedilol. Not only do these studies provide cellular mechanisms for the effects noted, they also indicate that carvedilol provides protection against hypertension as well as oxidative stress, which plays pivotal roles in endothelial dysfunction, fibrogenesis, and cardiovascular remodeling.