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Int Arch Allergy Immunol. 2008;146(1):71-5. Epub 2007 Dec 14.

Immediate hypersensitivity elicits renin release from cardiac mast cells.

Author information

1
Department of Pharmacology, Weill Cornell Medical College, New York, NY, USA.

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.

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.

PMID:
18087164
DOI:
10.1159/000112505
[Indexed for MEDLINE]

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