Accordingly, the integrity of the elastic fibers as well as the thickness of the muscular layer of the thoracic and abdominal aorta showed neither massive abnormalities nor differences between +TAM+Ang II-treated CTR and cmfKO mice (data not shown), although reportedly the architecture of the vessel wall can be disrupted by the development of aortic aneurysms in response to Ang II [68].We next monitored the BP of CTR and cmfKO mice because Ang II causes hypertension through different mechanisms, whereas the contribution of the cGMP/cGKI signaling pathway in CMF to BP control is less clear. The gene discussed is AGT; the disease is hypertensive disorder.