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Optical Mapping of Langendorff-perfused Rat Hearts
Published on: August 11, 2009
The Effect of Chemerin on Cardiac Parameters and Gene Expressions in Isolated Perfused Rat Heart
Özden Kutlay1, Ziya Kaygısız1, Bilgin Kaygısız2
1Department of Physiology, Eskişehir Osmangazi University School of Medicine, Eskişehir, Turkey
Insights
Chemerin negatively impacts cardiac function by reducing contractility and coronary flow in isolated rat hearts. This effect involves the nitric oxide pathway, CaV1.2, and PI3Kγ gene expression.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Adipokine Signaling
Background:
- Chemerin, a chemoattractant adipokine, is present in the cardiovascular system.
- Its receptor is found in epicardial adipose tissue, suggesting a role in cardiac function.
Purpose of the Study:
- To investigate the effects of chemerin on cardiac parameters and gene expression in an isolated perfused rat heart model.
- To elucidate the molecular mechanisms underlying chemerin's action on the heart.
Main Methods:
- Isolated rat hearts were perfused using the Langendorff technique.
- Hearts were treated with varying doses of chemerin (10-1000 nM) or a nitric oxide synthase inhibitor followed by chemerin.
- Real-time polymerase chain reaction was used to analyze gene expression of endothelial nitric oxide synthase, PI3Kγ, and CaV1.2.
Main Results:
- Chemerin significantly decreased left ventricular developed pressure and +dP/dtmax, indicating reduced cardiac contractility.
- Higher doses of chemerin reduced coronary flow.
- Chemerin increased endothelial nitric oxide synthase mRNA and cyclic guanosine monophosphate levels.
- Chemerin decreased PI3Kγ and CaV1.2 gene expression.
Conclusions:
- Acute chemerin administration exerts a negative inotropic effect on the isolated rat heart.
- The observed effects are mediated through the nitric oxide pathway, modulation of CaV1.2, and PI3Kγ gene expression.
Background:
Chemerin is a novel chemoattractant adipokine expressed in cardiovascular system, and its receptor has been detected in the epicardial adipose tissue.
Aims:
To determine the effects of chemerin on the cardiac parameters and gene expressions in the isolated perfused rat heart.
Study Design:
Animal experiment.
Methods:
The hearts were retrogradely perfused with Langendorff technique to measure the cardiac parameters. The experimental groups were acutely treated with 10, 100, and 1000 nM doses of chemerin. Another group was given 10 μM L-nitric oxide synthase inhibitor for 5 min before 1000 nM chemerin administration. The real-time polymerase chain reaction was performed for detecting the expression of target genes.
Results:
All doses of chemerin significantly decreased the left ventricular developed pressure (max 35.33 Δ%, p<0.001), and +dP/dtmax (max 31.3 Δ%, p<0.001), which are the indexes of cardiac contractile force. In addition, 1000 nM chemerin reduced the coronary flow (max 31 Δ%, p<0.001). N(W)-nitro-L-arginine methyl ester antagonized the negative inotropic effect of chemerin on contractility. Chemerin induced a 2.16-fold increase in endothelial nitric oxide synthase mRNA and increased the cyclic guanosine monophosphate levels (p<0.001) but decreased the PI3Kγ gene expression (1.8-fold, p<0.001). Furthermore, all doses of chemerin decreased the CaV1.2 gene expression (1.69-fold, p<0.001).
Conclusion:
Acute chemerin treatment induces a negative inotropic action with the involvement of nitric oxide pathway, CaV1.2, and PI3Kγ on isolated rat heart.
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