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Adrenaline inhibits macrophage nitric oxide production through β 1 and β 2 adrenergic receptors
Author(s) -
Sigola L. B.,
Zinyama R. B.
Publication year - 2000
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2000.00029.x
Subject(s) - atenolol , endocrinology , nitric oxide , agonist , phentolamine , chemistry , adrenergic receptor , medicine , phenylephrine , propranolol , receptor , prazosin , adrenergic antagonist , isoprenaline , yohimbine , pharmacology , antagonist , stimulation , blood pressure
Summary 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 β 1 and β 2 adrenergic receptors since isoprenaline (a non‐selective β 1 and β 2 agonist), dobutamine and salbutamol (selective β 1 and β 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 β blocker) and atenolol (a specific β 1 inhibitor). In contrast to β receptor activation, the α adrenergic agonist phenylephrine had no effect on the LPS NO response, and furthermore, phentolamine (an α receptor antagonist) did not ameliorate adrenaline’s inhibitory action.