title: Arterial remodeling in chronic sinoaortic-denervated rats.
abstract: The spontaneous variation of blood pressure is defined as "blood pressure variability" (BPV). The chronic sinoaortic-denervated (SAD) rat is a model of high BPV without sustained hypertension. Little is known about vascular remodeling in this model. In the present study, we examined blood pressure, vascular remodeling, and aortic angiotensin II concentration in chronic SAD rats in separate experiments. In experiment 1, intra-arterial blood pressure was continuously recorded in conscious unrestrained rats. The 16-week SAD rats had a significant increase in BPV and no change in the mean level of blood pressure over a 24-h period. In experiment 2, we measured structural changes of seven kinds of arteries by histologic method and computer image analysis and functional changes of thoracic aortas by isolated artery preparation. Structural remodeling after 16-week sinoaortic denervation was characterized by increase in wall thickness, wall area, and ratio of wall thickness to internal diameter, with different changes in internal diameter and external diameter in different arteries, indicating that arterial structural remodeling expresses itself mainly as vascular growth. This vascular growth might be caused by medial smooth muscle cell growth and collagen accumulation. Aortic contraction induced by norepinephrine was potentiated, whereas aortic relaxation induced by acetylcholine was attenuated after sinoaortic denervation. In experiment 3, plasma and aortic angiotensin II concentrations were determined by radioimmunoassay. The former remained unchanged, whereas the latter was significantly increased in 10-week SAD rats. It is concluded that in rats chronic sinoaortic denervation can produce vascular remodeling that might be related to increased BPV and an activated tissue renin-angiotensin system.
authors.affiliation: Department of Pharmacology, Basic Medical College, Second Military Medical University, Shanghai, China. cymiao@citiz.net
authors.forename: C Y
authors.initials: CY
authors.lastname: Miao
authors.forename: X
authors.initials: X
authors.lastname: Tao
authors.forename: K
authors.initials: K
authors.lastname: Gong
authors.forename: S H
authors.initials: SH
authors.lastname: Zhang
authors.forename: Z X
authors.initials: ZX
authors.lastname: Chu
authors.forename: D F
authors.initials: DF
authors.lastname: Su
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001011:Aorta / Q000294:innervation; D001158:Arteries / Q000473:pathology*; D001794:Blood Pressure / Q000502:physiology; D002346:Carotid Sinus / Q000294:innervation; D003714:Denervation; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000473:pathology*; D006984:Hypertrophy; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D000804:Angiotensin II