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1 Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA
* To whom correspondence should be addressed. E-mail: periasamy.1{at}osu.edu.
Genetically altered mice are increasingly used as experimental models. However, angiotensin (Ang) II responses in mouse blood vessels have not been well defined. Therefore, the aim of this study was to determine the role of Ang II in regulating major blood vessels in C57/BL6J mice using isometric force measurements. Results showed that in mouse abdominal aorta, Ang II induced a concentration-dependent contraction (EC50: 4.6 nM) with a maximum contraction of 75.1 ± 4.9% at 100 nM as compared with that of 60 mM K+. Similarly, femoral artery also exhibited a contractile response of 76.0 ± 3.4% to the maximum concentration of Ang II (100 nM). In contrast, Ang II (100 nM) induced contraction was significantly less in carotid artery (24.5 ± 6.6%) and only minimal (3.5 ± 0.31 %) in thoracic aorta. The nitric oxide synthase inhibitor L-NAME, or an AT2 antagonist PD-123319, failed to enhance Ang II induced contractions. However, an AT1 antagonist, losartan (10 µM) completely inhibited Ang II (100 nM) response in abdominal aorta and carotid artery. Meanwhile, an AT1 agonist, [Sar1]Ang II (100 nM) behaves similarly to Ang II (100 nM) in abdominal aorta and carotid artery. RT-PCR analyses showed that the mouse thoracic aorta has a significantly lower AT1 mRNA level than abdominal aorta. These results demonstrate that major mouse vessels exhibit differential contractions to Ang II, possibly because of varied AT1 receptor levels.
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