Role of calcitonin gene-related peptide in nitric oxide-mediated myocardial delayed preconditioning induced by heat stress

Citation
B. Tan et al., Role of calcitonin gene-related peptide in nitric oxide-mediated myocardial delayed preconditioning induced by heat stress, ACT PHAR SI, 22(9), 2001, pp. 851-856
Citations number
32
Categorie Soggetti
Pharmacology & Toxicology
Journal title
ACTA PHARMACOLOGICA SINICA
ISSN journal
02539756 → ACNP
Volume
22
Issue
9
Year of publication
2001
Pages
851 - 856
Database
ISI
SICI code
0253-9756(200109)22:9<851:ROCGPI>2.0.ZU;2-C
Abstract
AIM: To study the role of calcitonin gene-related peptide (CGRP) in nitric oxide (NO)-mediated myocardial delayed preconditioning induced by heat stre ss. METHODS: The isolated rat heart was perfused in a Langendorff model. He arts for all groups were subjected to 4 h hypothermia (4 degreesC) and 40 m in reperfusion (37 degreesC). In the hyperthemia-treated group, rats were s ubjected to whole-body hyperthermia ( rectal 42 degreesC, 15 min) 24 h befo re the experiment. Heart rate, coronary flow, left ventricular pressure, an d its derivative (+/- dp/dt(max)) were recorded, and calcitonin gene-relate d peptide-like immunoreactivity (CGRP-LI) in plasma and the activity of cre atine kinase (CK) in the coronary effluent were measured. RESULTS: Pretreat ment with hyperthermia significantly imporved the recovery of cardiac prote ction, reduced the release of CK, and increased plasma concentrations of CG RP. Pretreatment with L-NAME, an inhibitor of NOS, or capsaicin, which sele ctively depleted sensory neurotransmitter content, abolished the protective effects and the increased level of CGRP elicited by hyperthermia. CONCLUSI ON: Endogenous NO is involved in the cardioprotection afforded by heat stre ss, and the beneficial effects of NO are mediated by CGRP in the rat.