Changes of thoracic and mesenteric arterial vascular function in angiotensin Ⅱ-induced hypertensive mice

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  • Ito Masa-aki
    Lab. Pharmacol., Fact. Pharm, Takasaki Univ. Health and Welfare
  • Hayashi Takahiro
    Lab. Pharmacol., Fact. Pharm, Takasaki Univ. Health and Welfare
  • Koyama Teruaki
    Lab. Pharmacol., Fact. Pharm, Takasaki Univ. Health and Welfare
  • Yoshida Kazuki
    Lab. Pharmacol., Fact. Pharm, Takasaki Univ. Health and Welfare
  • Matsuoka Isao
    Lab. Pharmacol., Fact. Pharm, Takasaki Univ. Health and Welfare

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Other Title
  • アンジオテンシンⅡ誘発高血圧マウスにおける胸部および腸間膜動脈血管機能の変化

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<p>Endothelial cells play an important role in regulation of vascular function, which are affected by various bioactive substances. Angiotensin (Ang)Ⅱ induces vasoconstriction and is suggested to cause vascular dysfunction. In this study, we compared the endothelium-dependent vasorelaxation response of the thoracic aorta and mesenteric artery in AngⅡ-induced hypertensive model mice.</p><p>In thoracic aorta, stimulation of endothelial a2-adrenoceptor with clonidine induced a PI3-K-dependent relaxation, whereas acetylcholine (ACh) induced the relaxation via Gq-PLC-Ca2+ pathway. In mesenteric artery, ACh-induce relaxation was remarkable, but clonidine-induced relaxation was hardly observed. AngⅡ-induced hypertension significantly impaired the endothelium-dependent relaxation in aorta, but not in mesenteric artery. Experiment using NOS inhibitor revealed that vasorelaxation responses to clonidine and ACh in aorta were largely dependent on NOS activity, whereas NO played minor role in endothelial-dependent vasorelaxation in the mesenteric artery. These results suggest that NOS-dependent endothelial regulation of vascular tone is more sensitive to AngⅡ-induced vascular dysfunction. In addition, the difference in endothelium-dependent relaxation mechanism may be related to the susceptibility of distinct blood vessel to AngⅡ-induced vascular injury.</p>

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