Remodeled structure and reduced contractile responsiveness of ocular ciliary artery in spontaneously hypertensive rats
Remodeled structure and reduced contractile responsiveness of ocular ciliary artery in spontaneously hypertensive rats作者机构：Department of Ophthalmology the Second Hospital of Jilin University Department of Ophthalmology Akita University School of Medicine Division of Immunology and Rheumatology Department of Medicine Stanford University
出 版 物：《International Journal of Ophthalmology(English edition)》 (国际眼科杂志（英文版）)
年 卷 期：2019年第12卷第3期
页 面：363-368页
核心收录：
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 100212[医学-眼科学] 10[医学]
基 金：Supported by the Natural Science Foundation of China(No.81100695) the Japan Society for the Promotion of Science(JSPS)([C] 25462750)
主 题：remodeled structure contractile responsiveness ocular ciliary artery hypertension spontaneously hypertensive rat
摘 要：AIM: To investigate the alterations in both structure and contractile responsiveness of ocular ciliary artery(OCA) in spontaneously hypertensive rat(SHR).METHODS: In this experiment, 20-week-old male SHR and Wistar Kyoto rat(WKY) were studied. The heart rate(HR), the blood pressure(BP; the systolic BP and the diastolic BP) of rats with an electronic sphygmomanometer were measured. Vascular morphometry and isometric tension measurement were used to investigate the alterations in structure and contractility of ***: A general narrowing of OCAs was observed in SHR compared to the control WYK. In SHR, the media of OCAs were thicker, the luminal diameters were smaller, and the media-to-lumen ratios were higher when compared with WKY(P0.05). Indomethacin(10 μmol/L) decreased the contractions induced by norepinephrine in OCAs from WKY(P0.05).CONCLUSION: Our results demonstrate that the structure and function of OCAs are altered in hypertension. OCAs from SHR are remodeled with decreased lumen diameter and increased media-to-lumen ratio. Moreover, the contractile responsiveness of OCAs from SHR is diminished due to the disruption of vasoconstrictive effect of prostaglandins.
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