Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide

Adrenal hormone deprivation affects macrophage catecholamine metabolism and β2‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production

“…The study demonstrated that macrophages from both non‐operated and adrenalectomized rats exhibited a similar increase (∼320 pg ml −1 ) in LPS‐induced TNF‐α production following a 4 days of propranolol treatment. This modulatory effect of propranolol on TNF‐α production by macrophages further confirmed their catecholamine‐producing ability (Dimitrijević et al 2009) and suggested that catecholamines can modulate macrophage TNF‐α production by acting in an autocrine/paracrine manner. Furthermore, this study showed that macrophage‐derived catecholamines influence macrophage TNF‐α production through β 2 ‐adrenoceptors.…”

“…This suggested that the effects of β‐adrenoceptor blockade on TH and β 2 ‐adrenoceptor expression depend on the presence of adrenal gland hormones. In favour of ability of propranolol to augment β 2 ‐adrenoceptor expression in non‐operated rats are data that show the stimulatory effects of long‐lasting propranolol treatment on β 2 ‐adrenoceptor expression in peritoneal macrophages and some other cell types (Aarons et al 1980; Dimitrijević et al 2009). The increased TH expression in macrophage cells gated by light scatter/ED1 immunolabelling from non‐operated propranolol‐treated rats could be related to the data which indicate that a long‐lasting β‐adrenoceptor blockade affects TH activity, but depending on cell type, leads to differential effects (Peters & Mazurkiewicz‐Kwilecki, 1975; Raine & Chubb, 1977).…”

“…In addition, the capacity of the resting and lipopolysaccharide (LPS)‐stimulated RAW264.7 macrophage cell line and peritoneal mouse and rat macrophages to synthesize catecholamines has been acknowledged (Flierl et al 2007; Nguyen et al 2011). Several studies have shown that the blockade of α‐ and β‐adrenoceptors in vitro alters the ability of macrophages to produce reactive oxygen and nitrogen species and cytokines (Haskó et al 1998; Engler et al 2005; Dimitrijević et al 2009). This indicates that macrophage‐derived catecholamines, acting in an autocrine/paracrine manner, may exert modulatory influence on the production of inflammatory mediators by macrophages.…”

“…In addition, it has been demonstrated that glucocorticoids affect the expression of both β‐ and α 1 ‐adrenoceptors (Wolfe et al 1976; Day et al 1999). Given that β‐ and α‐adrenoceptor expressions are also influenced by catecholamines (Kavelaars, 2002; Dimitrijević et al 2009), it may be assumed that glucocorticoids may affect adrenoceptor expression by acting directly on cells, as well as by altering catecholamine bioavailability and, consequently, adrenoceptor expression.…”

“…Considering that propranolol may change surface α 1 ‐adrenoceptor expression of macrophages by affecting the β 2 ‐adrenoceptor‐mediated actions of catecholamines (Dimitrijević et al 2009), the production of this cytokine was also measured in the presence of a selective α 1 ‐adrenoceptor antagonist (prazosin). Prazosin did not affect LPS‐stimulated TNF‐α production in macrophage cultures (510 ± 30 pg ml −1 in the presence of 10 −6 prazosin versus 473 ± 30 pg ml −1 in the absence of prazosin; P > 0.05).…”