Abstract
Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects
against myocardial ischemia-reperfusion injury and that rutaecarpine activates vanilloid
receptors to evoke CGRP release. In the present study, we examined whether rutaecarpine
enhances preservation with cardioplegia in guinea-pig hearts, and whether the protective
effects of rutaecarpine are related to stimulation of endogenous CGRP release via
activating vanilloid receptors. The isolated guinea-pig heart was arrested using St.
Thomas Hospital solution, and then reperfused with normothermic Krebs-Henseleit solution
for 30 min after a 4-h hypothermic ischemic period. Hypothermic ischemia caused a
decline in cardiac function (left ventricular pressure, ±dp/dtmax , heart rate and coronary flow) and an increased release of creatine kinase during
reperfusion. Rutaecarpine at the concentration of 1.0 μM significantly improved the
recovery of cardiac function and reduced the release of creatine kinase during reperfusion
after hypothermic ischemia. Rutaecarpine at the concentration of 3.0 μM significantly
reduced the release of creatine kinase and increased the coronary flow, but only caused
a slight improvement of left ventricular pressure, ±dp/dtmax , heart rate during reperfusion. The cardioprotective effects of rutaecarpine were
abolished by capsazepine, a competitive vanilloid receptor antagonist, or by CGRP
(8-37), a selective CGRP receptor antagonist. Rutaecarpine at the concentration of
1.0 or 3.0 μM significantly increased the release of CGRP, which was also abolished
by capsazepine. These results suggest that rutaecarpine enhances preservation with
cardioplegia in guinea-pig hearts and that the protective effects of rutaecarpine
are due to stimulation of endogenous CGRP release via activating vanilloid receptors.
Key words
Evodia rutaecarpa
- Rutaceae - rutaecarpine - calcitonin gene-related peptide - vanilloid receptor -
capsaicin - guinea-pig isolated heart
References
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LiYJ@public.cs.hn.cn
