The effects of angiotensin II signaling pathway in the systolic response to acute stretch in the normal and ischemic myocardium

• Type: Article in International Scientific Journal
• Date: 2013

Authors

Neves, JS (Author) FMUP; Castro Ferreira, R (Author) Other; Ladeiras-Lopes R (Author) FMUP; Neiva Sousa, M (Author) Other; Leite Moreira, AM (Author) FMUP; Almeida Coelho, J (Author) Other; Fontes-Carvalho R (Author) FMUP; Ferreira-Martins J (Author) FMUP; Leite-Moreira AF (Author) FMUP

Journal

Title: Peptides

Vol. 47

Pages: 77-84

ISSN: 0196-9781

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 9 Citations

Scopus - 10 Citations

Other information

Authenticus ID: P-006-7R0

DOI: 10.1016/j.peptides.2013.07.004

Abstract (EN): Acute myocardial stretch elicits a biphasic increase in contractility: an immediate increase, known as Frank-Starling mechanism (FSM), followed by a progressive increase, regarded as slow force response (SFR). In this study, we characterized the contractile response to acute stretch from 92 to 100% L-max in rabbit papillary muscles (n = 86) under normoxic and ischemic conditions, and its modulation by angiotensin II signaling pathway. Under normoxia, the FSM was independent of Na+/H+-exchanger, reverse mode of Na+/Ca2+-exchanger (r-NCX), AT1 receptor, AT2 receptor and PKC. Regarding the SFR, it was mediated by AT1 receptor activation and its downstream effectors PKC, Na+/H+-exchanger and r-NCX. Ischemia negatively impacted on the FSM and abolished the SFR, with the muscles exhibiting a time-dependent decline in contractility. Under ischemic conditions, FSM was not influenced by AT1 and AT2 receptors or PKC activation. AT1 receptor antagonism rescued the progressive deterioration in contractility, an effect partially dependent on AT2 receptor activation.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 8