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1 Deparment of Physiology and Cell Biology, The Ohio State University, College of Medicine and Public Health, Columbus, OH, USA; Davis Heart & Lung Research Institute, The Ohio State University, College of Medicine and Public Health, Columbus, OH, USA
2 Deparment of Physiology and Cell Biology, The Ohio State University, College of Medicine and Public Health, Columbus, OH, USA
3 Davis Heart & Lung Research Institute, The Ohio State University, College of Medicine and Public Health, Columbus, OH, USA
* To whom correspondence should be addressed. E-mail: periasamy.1{at}osu.edu.
Mice have been increasingly used as models for investigating cardiovascular diseases. However,
the responsiveness of mouse vasculature to endothelin (ET)-1 has not been clearly established. The goal of this study was to determine the role of ET receptors (ETA and ETB) in mouse vessels using isometric force measurements. Results showed that in the abdominal aorta ET-1 induced a
concentration-dependent contraction (EC50: 1.4 nM) with maximum reaching 89.5 ± 4.9% (10 nM) of that induced by 60 mM K+ [with nitric oxide synthase (NOS) inhibitor N
-nitro-L-arginine methyl ester (L-NAME)]. However in the thoracic aorta or the carotid artery, ET-1 was poorly effective. RT-PCR revealed that in the endothelium-denuded abdominal aorta, the PCR product
for ETB receptors was very low compared to ETA. Similarly in tissues treated with L-NAME, the ETB receptor-specific agonist sarafotoxin 6c (S6c; 100 nM) induced only a minimal contraction (less than 5%). Meanwhile, the ETA antagonist BQ-123 (1 µM) completely inhibited the maximum ET-1 (10 nM) contractile response. Furthermore, we found that in the abdominal aorta that had not been treated with L-NAME, ET-1 induced contraction significantly decreased.
However in such specimens, S6c was unable to induce any relaxation on phenylephrine-induced contraction. These results indicate that the role of ET receptors differs considerably among mouse vessels. In the abdominal aorta, ETA receptor mediates a potent vasoconstrictor response, while ETB has, if any, only a minimal functional presence. Also, our data suggest that ET-1 might involve a NOS-dependent vasodilation in the abdominal aorta, which remains to be further defined.
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