TY - JOUR
T1 - Beta adrenoceptor regulation of macrophage arginase activity
AU - Bernard, Andrew C.
AU - Fitzpatrick, Elizabeth A.
AU - Maley, Mary E.
AU - Gellin, Gloria L.
AU - Tsuei, Betty J.
AU - Arden, Warwick A.
AU - Boulanger, Bernard R.
AU - Kearney, Paul A.
AU - Ochoa, Juan B.
N1 - Funding Information:
Supported in part by a grant from the Southern Medical Association.
PY - 2000
Y1 - 2000
N2 - Background. Arginase, which metabolizes L-arginine within the urea cycle, is essential for production of polyamines and affects production of nitric oxide by depletion of L-arginine, the common substrate for both arginase and nitric oxide synthase. Having shown that trauma increases splenic macrophage arginase activity, we seek to define the mechanisms for this. RAW macrophage arginase activity and expression are increased by 8- bromo-cAMP in vitro. We hypothesize that since catecholamines increase cAMP, trauma-induced splenic arginase activity may be mediated by post-injury catecholamine release. Methods. RAW 264.7 macrophage arginase activity was measured in vitro in response to 4 catecholamines with or without propranolol or lipopolysaccharide (LPS). C57BL/6 mice underwent laparotomy as a model of moderate trauma after propranolol treatment, with and without intraperitoneal Escherichia coli LPS administration as a simulated pro-inflammatory stimulus. Results. Macrophage arginase activity increased in vitro in response to catecholamines or LPS (P <. 05). Propranolol pretreatment blocked macrophage arginase activity induced by epinephrine (10 μmol/L) in vitro (P <. 05). Trauma or LPS alone increased splenic arginase activity in vivo (P <. 05). Propranolol did not alter LPS-induced splenic arginase activity but did significantly reduce trauma-induced splenic arginase activity (P < .05). Conclusions. Catecholamines alone increase macrophage arginase activity through β-adrenoceptor activation. Increased splenic arginase activity induced by moderate trauma is decreased by β-adrenoceptor blockade, suggesting that trauma-induced arginase activity is partly mediated by endogenous catecholamines.
AB - Background. Arginase, which metabolizes L-arginine within the urea cycle, is essential for production of polyamines and affects production of nitric oxide by depletion of L-arginine, the common substrate for both arginase and nitric oxide synthase. Having shown that trauma increases splenic macrophage arginase activity, we seek to define the mechanisms for this. RAW macrophage arginase activity and expression are increased by 8- bromo-cAMP in vitro. We hypothesize that since catecholamines increase cAMP, trauma-induced splenic arginase activity may be mediated by post-injury catecholamine release. Methods. RAW 264.7 macrophage arginase activity was measured in vitro in response to 4 catecholamines with or without propranolol or lipopolysaccharide (LPS). C57BL/6 mice underwent laparotomy as a model of moderate trauma after propranolol treatment, with and without intraperitoneal Escherichia coli LPS administration as a simulated pro-inflammatory stimulus. Results. Macrophage arginase activity increased in vitro in response to catecholamines or LPS (P <. 05). Propranolol pretreatment blocked macrophage arginase activity induced by epinephrine (10 μmol/L) in vitro (P <. 05). Trauma or LPS alone increased splenic arginase activity in vivo (P <. 05). Propranolol did not alter LPS-induced splenic arginase activity but did significantly reduce trauma-induced splenic arginase activity (P < .05). Conclusions. Catecholamines alone increase macrophage arginase activity through β-adrenoceptor activation. Increased splenic arginase activity induced by moderate trauma is decreased by β-adrenoceptor blockade, suggesting that trauma-induced arginase activity is partly mediated by endogenous catecholamines.
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U2 - 10.1067/msy.2000.104115
DO - 10.1067/msy.2000.104115
M3 - Article
C2 - 10776432
AN - SCOPUS:0034000911
SN - 0039-6060
VL - 127
SP - 412
EP - 418
JO - Surgery
JF - Surgery
IS - 4
ER -