Epinephrine promotes pulmonary angiitis: evidence for a 1-adrenoreceptor-mediated mechanism

Jain, Felipe A., Long-hai Zhao, Martin K. Selig, and Richard L. Kradin. Epinephrine promotes pulmonary angiitis: evidence for a 1-adrenoreceptor-mediated mechanism. Am J Physiol Lung Cell Mol Physiol 285: L232–L239, 2003; 10.1152/ajplung.00248.2002.—Epinephrine (Epi) increases lymphocyte traffic to lung. We investigated whether Epi also modulates pulmonary cell-mediated immune responses in vivo. C57BL/6 mice were immunized with hen-egg lysozyme (HEL) on day 0, challenged with HEL intratracheally at day 12, and killed at day 15. Mice received Epi (0.5 mg/kg) subcutaneously during the sensitization phase, days 1–7 (Epi-SP), or the effector phase, days 12–14 (Epi-EP); controls received saline subcutaneously. Epi-SP mice showed increased airway inflammation (P 0.03) and pulmonary angiitis (P 0.04) characterized by endothelialitis and subendothelial fibrin deposition. Macrophages and granulocytes were increased in perivascular cuffs in situ (P 0.001). CD3 lymphocytes increased in the bronchoalveolar lavage fluid, whereas NK1.1 and CD4 CD25 lymphocytes decreased (all P 0.05). Atenolol, a selective 1-adrenoreceptor (AR) antagonist, inhibited the increased vascular and airway inflammation and the reduction in CD4 CD25 lymphocytes (all P 0.05) yielded by Epi, whereas all / -AR blockers inhibited airway inflammation. We conclude that Epi-EP selectively promotes vascular inflammation in vivo via a 1-receptor-mediated mechanism.