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Adrenaline inhibits macrophage nitric oxide production through beta1 and beta2 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 beta1 and beta2 adrenergic receptors since isoprenaline (a non-selective beta1 and beta2 agonist), dobutamine and salbutamol (selective beta1 and beta2 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 beta1 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.