血管紧张素ii诱导Fischer 344和Wistar Kyoto大鼠血压和结构变化的比较。

IF 2.4 4区 医学 Q3 PHARMACOLOGY & PHARMACY
Jocelyne Blanc, Patrick Lacolley, Stéphane Laurent, Jean-Luc Elghozi
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引用次数: 1

摘要

1. 本研究的目的是评价Fischer 344 (F344)大鼠与Wistar Kyoto (WKY)大鼠在慢性血管紧张素(Ang) II输注时的血压(BP)反应、惊吓反应的BP和心率(HR)成分以及颈动脉和主动脉的结构。2. 8周龄正常大鼠皮下注入生理盐水或AngII (120 ng/kg / min)的渗透微型泵,F344大鼠皮下注入4周(生理盐水,n = 10;AngII大鼠,n = 10)和WKY大鼠(生理盐水,n = 10;记录清醒大鼠的基础血压、心率和对持续时间为0.7 s、115 dB的声惊吓刺激的反应。在4%甲醛固定的动脉中测定颈动脉和主动脉的结构。3.与WKY大鼠相比,F344灌胃大鼠体重(BW;266 +/- 7 vs 299 +/- 9 g;P < 0.05)和心脏重量(0.80 +/- 0.02 vs 0.98 +/- 0.04 g;P < 0.05),主动脉收缩压升高(SBP;131 +/- 1 vs 123 +/- 5 mmHg;P < 0.001)和舒张压(98 +/- 3 vs 89 +/- 2 mmHg;P < 0.001)。F344大鼠颈动脉壁厚/体重比较WKY大鼠增加(156 +/- 9 vs 131 +/- 6 nm/g;P < 0.05)和腹主动脉(264 +/- 13 vs 217 +/- 12 nm/g;P < 0.05),且胸主动脉血管内血管密度降低(246 +/- 13 vs 275 +/- 8 nm/g;P < 0.05)。弹性蛋白和胶原蛋白密度无显著差异。血管紧张素II对F344和WKY大鼠的血压有显著的提高(SBP分别为163 +/- 5和132 +/- 4 mmHg);P(菌株x处理)< 0.05)。与WKY大鼠相比,F344大鼠主动脉环壁应力增加(胸、腹主动脉分别为1176 +/- 39 vs 956 +/- 12 kPa (P < 0.001)和1107 +/- 42 vs 813 +/- 12 kPa (P < 0.001))。F344大鼠的惊吓反应被放大,与WKY大鼠的反应相比,SBP和脉压(PP)和心动过缓增加(F344大鼠分别为+44 +/- 9 mmHg, +10 +/- 2 mmHg和-40 +/- 17 b.p.m.,而WKY大鼠分别为+28 +/- 4 mmHg, +4 +/- 2 mmHg和-19 +/- 10 b.p.m.;BP和PP P(菌株)< 0.05)。惊吓反应不受AngII的影响。4. 这些结果表明,与WKY大鼠相比,F344大鼠的血压升高导致壁厚增加。我们认为,交感神经活动的增加导致了这些血流动力学差异,正如在声惊吓刺激期间血压过度增加所表明的那样。血管紧张素II增加了F344大鼠的血压,但在惊吓反应中没有夸大血压的增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Comparison of angiotensin II-induced blood pressure and structural changes in Fischer 344 and Wistar Kyoto rats.

1. The purpose of the present study was to evaluate the blood pressure (BP) response, the BP and heart rate (HR) components of the startle reaction and the structure of the carotid artery and the aorta during chronic infusion of angiotensin (Ang) II in Fischer 344 (F344) compared with Wistar Kyoto (WKY) rats, two in-bred normotensive contrasted strains. 2. Osmotic mini-pumps filled with saline vehicle or AngII (120 ng/kg per min) were implanted subcutaneously in 8-week-old normotensive rats and infused for 4 weeks in F344 rats (saline, n = 10; AngII, n = 10) and WKY rats (saline, n = 10; AngII, n = 9). Basal BP, HR and the responses to an acoustic startle stimulus (duration 0.7 s, 115 dB) were recorded in conscious rats. The structure of the carotid artery and aorta was determined in 4% formaldehyde-fixed arteries. 3. Compared with WKY rats, vehicle-treated F344 rats had lower bodyweight (BW; 266 +/- 7 vs 299 +/- 9 g; P < 0.05) and heart weight (0.80 +/- 0.02 vs 0.98 +/- 0.04 g; P < 0.05) and higher aortic systolic BP (SBP; 131 +/- 1 vs 123 +/- 5 mmHg; P < 0.001) and diastolic BP (98 +/- 3 vs 89 +/- 2 mmHg; P < 0.001). In F344 rats, compared with the WKY rats, the wall thickness/BW ratio was increased in the carotid artery (156 +/- 9 vs 131 +/- 6 nm/g; P < 0.05) and abdominal aorta (264 +/- 13 vs 217 +/- 12 nm/g; P < 0.05) and decreased in the thoracic aorta (246 +/- 13 vs 275 +/- 8 nm/g; P < 0.05). There was no difference in elastin and collagen density. Angiotensin II differentially enhanced BP in both strains: (SBP: 163 +/- 5 and 132 +/- 4 mmHg in F344 and WKY rats, respectively; P(strain x treatment) < 0.05). Circumferential wall stress was increased in the aorta of F344 rats compared with WKY rats (1176 +/- 39 vs 956 +/- 12 kPa (P < 0.001) and 1107 +/- 42 vs 813 +/- 12 kPa (P < 0.001) in thoracic and abdominal aortas, respectively). The startle response was amplified in F344 rats, with enhanced increases in SBP and pulse pressure (PP) and bradycardia compared with responses of WKY rats (+44 +/- 9 mmHg, +10 +/- 2 mmHg and -40 +/- 17 b.p.m., respectively, in F344 rats vs+28 +/- 4 mmHg, + 4 +/- 2 mmHg and -19 +/- 10 b.p.m. in WKY rats, respectively; P(strain) < 0.05 for BP and PP). The startle response was not affected by AngII. 4. These results indicate a higher BP producing an increase in wall thickness in F344 rats compared with WKY rats. We propose that an increase in sympathetic nervous activity causes these haemodynamic differences, as suggested by the excessive increase in BP during an acoustic startle stimulus. Angiotensin II increased BP in F344 rats, but did not exaggerate the increase in BP during the startle reaction.

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来源期刊
Clinical and Experimental Pharmacology and Physiology
Clinical and Experimental Pharmacology and Physiology PHARMACOLOGY & PHARMACY-PHYSIOLOGY
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期刊介绍: Clinical and Experimental Pharmacology and Physiology is an international journal founded in 1974 by Mike Rand, Austin Doyle, John Coghlan and Paul Korner. Our focus is new frontiers in physiology and pharmacology, emphasizing the translation of basic research to clinical practice. We publish original articles, invited reviews and our exciting, cutting-edge Frontiers-in-Research series’.
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