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Immediate Hypersensitivity Elicits Renin Release from Cardiac Mast Cells

Kano S.a · Tyler E.a · Salazar-Rodriguez M.a · Estephan R.a · Mackins C.J.a · Veerappan A.b · Reid A.C.b · Silver R.B.b · Levi R.a
Departments of aPharmacology and bPhysiology and Biophysics, Weill Cornell Medical College, New York, N.Y., USA Int Arch Allergy Immunol 2008;146:71–75 (DOI:10.1159/000112505)


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. Methods: Hearts isolated from presensitized guinea pigs were challenged with antigen. Results: Cardiac anaphylaxis was characterized by mast cell degranulation, evidenced by β-hexosaminidase release and associated with renin and norepinephrine release. Mast cell stabilization with cromolyn or lodoxamide markedly attenuated the release of β-hexosaminidase, renin and norepinephrine. Renin inhibition with BILA2157 did not affect mast cell degranulation, but attenuated norepinephrine release. 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.


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