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B‐type Natriuretic Peptide and EET Mediated Cardioprotection
Author(s) -
Chaudhary Ketul,
Batchu Sri Nagarjun,
Das Dipankar,
Suresh Mavanur,
Graves Joan,
Zeldin Darryl C,
Seubert John M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.479.43
Subject(s) - cardioprotection , natriuretic peptide , medicine , glibenclamide , antagonist , endocrinology , chemistry , perfusion , ischemia , receptor , heart failure , diabetes mellitus
B‐type natriuretic peptide (BNP) can attenuate ischemic‐reperfusion injury through natriuretic peptide receptor type‐A (NPR‐A). We investigated the role of BNP in epoxyeicosatrienoic acids(EET) mediated cardioprotection. Hearts from sEH null (KO), littermate controls(WT) and C57 mice were perfused in a Langendorff apparatus and subjected to 20/30min of ischemia followed by 40min of reperfusion. RT‐PCR analysis for preproBNP (Nppb) mRNA expression was performed in both naïve and isolated perfused hearts. Relative to naïve hearts, KO mice had a significant increase in Nppb mRNA expression following both preischemic perfusion (KO 5‐fold; WT 2‐fold) and postischemic reperfusion (KO 19‐fold; WT 7‐fold), correlating with improved postischemic left ventricular (LV) function (KO 52±3; WT 23.1±3%). K ATP channel blocker, glibenclamide(1μM), and an EET antagonist, 14,15‐EEZE (1μM), significantly reduced the expression of mRNA in KO hearts compared to vehicle controls. Addition of exogenous BNP or EETs resulted in significant increases in LV functional recovery (BNP 59.2±13, EET 54.4±21, control 23.1±3%). BNP‐mediated protection was abolished with co‐administration of 14,15‐EEZE or A71915 (NPR‐A antagonist) (14,15‐EEZE 18.3±10, A71915 39.7±19%). However, EET‐mediated effects were not affected by A71915 (48.5±25%). Our results suggest a correlation between BNP and EET‐mediated cardioprotection.