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Updated: Jul 9, 2026

Humanized Mediator Release Assay as a Read-Out for Allergen Potency
Published on: June 29, 2021
Immediate hypersensitivity elicits renin release from cardiac mast cells
Seiichiro Kano1, Eleanor Tyler, Mariselis Salazar-Rodriguez
1Department of Pharmacology, Weill Cornell Medical College, New York, NY, USA.
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 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.
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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