Selective Deletion of the Brain-Specific Isoform of Renin Causes Neurogenic Hypertension.

ABSTRACT: The renin-angiotensin system (RAS) in the brain is a critical determinant of blood pressure, but the mechanisms regulating RAS activity in the brain remain unclear. Expression of brain renin (renin-b) occurs from an alternative promoter-first exon. The predicted translation product is a nonsecreted enzymatically active renin whose function is unknown. We generated a unique mouse model by selectively ablating the brain-specific isoform of renin (renin-b) while preserving the expression and function of the classical isoform expressed in the kidney (renin-a). Preservation of renal renin was confirmed by measurements of renin gene expression and immunohistochemistry. Surprisingly, renin-b-deficient mice exhibited hypertension, increased sympathetic nerve activity to the kidney and heart, and i

SUBMITTER: Shinohara K 

PROVIDER: S-EPMC5159235 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature