Hypoxia-Inducible Factor-1α Mediates Increased Sympathoexcitation via Glutamatergic N-Methyl-d-Aspartate Receptors in the Paraventricular Nucleus of Rats With Chronic Heart Failure.

ABSTRACT:

Background

Increased sympathetic outflow is a major contributor to the progression of chronic heart failure (CHF). Potentiation of glutamatergic tone has been causally related to the sympathoexcitation in CHF. Specifically, an increase in the N-methyl-d-aspartate-type 1 receptor (NMDA-NR₁) expression within the paraventricular nucleus (PVN) is critically linked to the increased sympathoexcitation during CHF. However, the molecular mechanism(s) for the upregulation of NMDA-NR₁ remains unexplored. We hypothesized that hypoxia via hypoxia-inducible factor 1α (HIF-1α) might contribute to the augmentation of the NMDA-NR₁-mediated sympathoexcitatory responses from the PVN in CHF.

Methods and results

Immunohistochemistry staining, mRNA, and protein

SUBMITTER: Sharma NM 

PROVIDER: S-EPMC5123857 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature