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