Adrenaline inhibits macrophage nitric oxide production through β1 and β2 adrenergic receptors

This study was conducted to investigate the role of the acute stress hormone adrenaline on macrophage nitric oxide (NO) production. Murine peritoneal macrophages were stimulated in vitro with lipopolysaccharide (LPS) in the absence or presence of adrenaline. Adrenaline inhibited the LPS-induced nitrite response in a dose-dependent manner. The suppressive effect of adrenaline on NO production was mediated via beta(1) and beta(2) adrenergic receptors since isoprenaline (a non-selective beta(1) and beta(2) agonist), dobutamine and salbutamol (selective beta(1) and beta(2) agonists, respectively) had similar effects on the NO response. In addition, the inhibitory effect of adrenaline on NO was abrogated by both propranolol (a non-specific beta blocker) and atenolol (a specific beta(1) inhibitor). In contrast to beta receptor activation, the alpha adrenergic agonist phenylephrine had no effect on the LPS NO response, and furthermore, phentolamine (an alpha receptor antagonist) did not ameliorate adrenaline's inhibitory action.