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

AIM

To study the role of calcitonin gene-related peptide (CGRP) in nitric oxide (NO)-mediated myocardial delayed preconditioning induced by heat stress.

METHODS

The isolated rat heart was perfused in a Langendorff model. Hearts for all groups were subjected to 4 h hypothermia (4 degrees C) and 40 min reperfusion (37 degrees C). In the hyperthermia-treated group, rats were subjected to whole-body hyperthermia (rectal 42 degrees C, 15 min) 24 h before the experiment. Heart rate, coronary flow, left ventricular pressure, and its derivative (+/- dp/dtmax) were recorded, and calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) in plasma and the activity of creatine kinase (CK) in the coronary effluent were measured.

RESULTS

Pretreatment with hyperthermia significantly improved the recovery of cardiac protection, reduced the release of CK, and increased plasma concentrations of CGRP. Pretreatment with L-NAME, an inhibitor of NOS, or capsaicin, which selectively depleted sensory neurotransmitter content, abolished the protective effects and the increased level of CGRP elicited by hyperthermia.

CONCLUSION

Endogenous NO is involved in the cardioprotection afforded by heat stress, and the beneficial effects of NO are mediated by CGRP in the rat.