B-type natriuretic peptide is upregulated by c-Jun N-terminal kinase and contributes to septic hypotension.

ABSTRACT: B-type natriuretic peptide (BNP) is secreted by ventricular cardiomyocytes in response to various types of cardiac stress and has been used as a heart failure marker. In septic patients, increased BNP suggests poor prognosis; however, no causal link has been established. Among various effects, BNP decreases systemic vascular resistance and increases natriuresis that leads to lower blood pressure. We previously observed that JNK inhibition corrects cardiac dysfunction and suppresses cardiac BNP mRNA in endotoxemia. In this study, we investigated the transcriptional mechanism that regulates BNP expression and the involvement of plasma BNP in causing septic hypotension. Our in vitro and in vivo findings confirmed that activation of JNK signaling increases BNP expression in sepsis via direct b

SUBMITTER: Hoffman M 

PROVIDER: S-EPMC7205432 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature