Central nervous system circuits modified in heart failure: pathophysiology and therapeutic implications

• Type: Article in International Scientific Journal
• Date: 2014

Authors

Sousa Pinto, B (Author) Other; Ferreira Pinto, MJ (Author) FMUP; Santos, M (Author) Other; Leite-Moreira AF (Author) FMUP

Journal

Title: Heart Failure Reviews

Vol. 19

Pages: 759-779

ISSN: 1382-4147

Publisher: Springer Nature

Indexing

ISI Web of Knowledge - 13 Citations

Scopus - 12 Citations

Other information

Authenticus ID: P-009-XGC

DOI: 10.1007/s10741-014-9427-x

Abstract (EN): The pathophysiology of heart failure (HF) is characterized by an abnormal activation of neurohumoral systems, including the sympathetic nervous and the renin-angiotensin-aldosterone systems, which have long-term deleterious effects on the disease progression. Perpetuation of this neurohumoral activation is partially dependent of central nervous system (CNS) pathways, mainly involving the paraventricular nucleus of the hypothalamus and some regions of the brainstem. Modifications in these integrative CNS circuits result in the attenuation of sympathoinhibitory and exacerbation of sympathoexcitatory pathways. In addition to the regulation of sympathetic outflow, these central pathways coordinate a complex network of agents with an established pathophysiological relevance in HF such as angiotensin, aldosterone, and proinflammatory cytokines. Central pathways could be potential targets in HF therapy since the current mainstay of HF pharmacotherapy aims primarily at antagonizing the peripheral mechanisms. Thus, in the present review, we describe the role of CNS pathways in HF pathophysiology and as potential novel therapeutic targets.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 21