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Immediate hypersensitivity elicits renin release from cardiac mast cells.

Authors :: Kano S
Tyler E
Salazar-Rodriguez M
Estephan R
Mackins CJ
Veerappan A
Reid AC
Silver RB
Levi R
Source :: International archives of allergy and immunology [Int Arch Allergy Immunol] 2008; Vol. 146 (1), pp. 71-5. Date of Electronic Publication: 2007 Dec 14.
Publication Year :: 2008
Abstract: Background: We recently reported that murine and cavian heart mast cells are a unique extrarenal source of renin. Ischemia/reperfusion releases this renin leading to local angiotensin formation and norepinephrine release. As mast cells are a primary target of hypersensitivity, we assessed whether anaphylactic mast cell degranulation also results in renin and norepinephrine release.<br />Methods: Hearts isolated from presensitized guinea pigs were challenged with antigen.<br />Results: Cardiac anaphylaxis was characterized by mast cell degranulation, evidenced by beta-hexosaminidase release and associated with renin and norepinephrine release. Mast cell stabilization with cromolyn or lodoxamide markedly attenuated the release of beta-hexosaminidase, renin and norepinephrine. Renin inhibition with BILA2157 did not affect mast cell degranulation, but attenuated norepinephrine release.<br />Conclusions: Our findings disclose that immediate-type hypersensitivity elicits renin release from mast cells, activating a local renin-angiotensin system, thereby promoting norepinephrine release. As renin is stored in human heart mast cells, allergic reactions could initiate renin release, leading to local angiotensin formation and hyperadrenergic dysfunction.<br /> (Copyright 2007 S. Karger AG, Basel.)