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Hypertension in Obese Black Women is Not Caused by Increased Sympathetic Vascular Tone.肥胖黑人女性的高血压不是由交感血管紧张增加引起的。
J Am Heart Assoc. 2017 Nov 18;6(11):e006971. doi: 10.1161/JAHA.117.006971.
2
Enhanced Endothelin-1 Mediated Vasoconstriction of the Ophthalmic Artery May Exacerbate Retinal Damage after Transient Global Cerebral Ischemia in Rat.增强的内皮素-1介导的眼动脉血管收缩可能会加重大鼠短暂性全脑缺血后的视网膜损伤。
PLoS One. 2016 Jun 20;11(6):e0157669. doi: 10.1371/journal.pone.0157669. eCollection 2016.
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Neural Control of Non-vasomotor Organs in Hypertension.高血压中非血管运动器官的神经控制
Curr Hypertens Rep. 2016 Apr;18(4):30. doi: 10.1007/s11906-016-0635-8.
4
Dorzolamide-induced relaxation of isolated rabbit ciliary arteries mediated by inhibition of extracellular calcium influx.多佐胺通过抑制细胞外钙内流介导离体兔睫状动脉舒张。
Jpn J Ophthalmol. 2016 Mar;60(2):103-10. doi: 10.1007/s10384-015-0423-z. Epub 2016 Jan 12.
5
Low-salt diet increases NO bioavailability and COX-2 vasoconstrictor prostanoid production in spontaneously hypertensive rats.低盐饮食会增加自发性高血压大鼠体内一氧化氮(NO)的生物利用度以及环氧化酶-2(COX-2)血管收缩性前列腺素的生成。
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Cerebrospinal Fluid Hypernatremia Elevates Sympathetic Nerve Activity and Blood Pressure via the Rostral Ventrolateral Medulla.脑脊液高钠血症通过延髓头端腹外侧区升高交感神经活性和血压。
Hypertension. 2015 Dec;66(6):1184-90. doi: 10.1161/HYPERTENSIONAHA.115.05936. Epub 2015 Sep 28.
7
Malignant hypertension: clinical manifestations of 7 cases.恶性高血压:7例临床表现
Klin Monbl Augenheilkd. 2015 Apr;232(4):590-2. doi: 10.1055/s-0034-1396333. Epub 2015 Apr 22.
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Nonarteritic anterior ischemic optic neuropathy in young patients.
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9
The sympathetic nervous system alterations in human hypertension.人类高血压中的交感神经系统改变。
Circ Res. 2015 Mar 13;116(6):976-90. doi: 10.1161/CIRCRESAHA.116.303604.
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Endothelium-derived Relaxing Factors of Small Resistance Arteries in Hypertension.高血压中小阻力动脉内皮衍生的舒张因子。
Toxicol Res. 2014 Sep;30(3):141-8. doi: 10.5487/TR.2014.30.3.141.

自发性高血压大鼠眼睫状动脉结构重塑及收缩反应性降低

Remodeled structure and reduced contractile responsiveness of ocular ciliary artery in spontaneously hypertensive rats.

作者信息

Dong Ya-Ru, Gustafson Claire E, Wang Jun, Cui Ji-Zhe, Yoshitomi Takeshi

机构信息

Department of Ophthalmology, the Second Hospital of Jilin University, Changchun 130041, Jilin Province, China.

Department of Ophthalmology, Akita University School of Medicine, Akita 010-8543, Japan.

出版信息

Int J Ophthalmol. 2019 Mar 18;12(3):363-368. doi: 10.18240/ijo.2019.03.02. eCollection 2019.

DOI:10.18240/ijo.2019.03.02
PMID:30918801
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6423402/
Abstract

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 OCA.

RESULTS

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 (<0.05). The contractions of OCAs evoked by norepinephrine were smaller in SHR compared to control (<0.05). Then, OCAs were pretreated with iberiotoxin, L-NAME, or indomethacin 30min before norepinephrine-induced contraction. Iberiotoxin (0.1 µmol/L) has not changed the norepinephrine-induced contractions in OCAs from both groups. However, L-NAME (100 µmol/L) increased the vasoconstrictions, the increased extents were similar in SHR and WKY (>0.05). Indomethacin (10 µmol/L) decreased the contractions induced by norepinephrine in OCAs from WKY (<0.05), but did not change those contractions in vessels from SHR (>0.05).

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.

摘要

目的

研究自发性高血压大鼠(SHR)眼睫状动脉(OCA)的结构和收缩反应性变化。

方法

本实验研究20周龄雄性SHR和Wistar Kyoto大鼠(WKY)。用电子血压计测量大鼠的心率(HR)、血压(BP;收缩压和舒张压)。采用血管形态测量和等长张力测量来研究OCA的结构和收缩性变化。

结果

与对照WKY相比,SHR的OCA普遍变窄。与WKY相比,SHR的OCA中膜更厚,管腔直径更小,中膜与管腔比值更高(<0.05)。与对照组相比,SHR中去甲肾上腺素诱发的OCA收缩较小(<0.05)。然后,在去甲肾上腺素诱发收缩前30分钟,用iberiotoxin、L-NAME或吲哚美辛预处理OCA。iberiotoxin(0.1 μmol/L)未改变两组OCA中去甲肾上腺素诱发的收缩。然而,L-NAME(100 μmol/L)增加了血管收缩,SHR和WKY中的增加程度相似(>0.05)。吲哚美辛(10 μmol/L)降低了WKY的OCA中去甲肾上腺素诱发的收缩(<0.05),但未改变SHR血管中的这些收缩(>0.05)。

结论

我们的结果表明,高血压时OCA的结构和功能发生改变。SHR的OCA发生重塑,管腔直径减小,中膜与管腔比值增加。此外,由于前列腺素血管收缩作用的破坏,SHR的OCA收缩反应性降低。