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4周龄自发性高血压大鼠肠系膜床和主动脉环对内皮素-1的敏感性和反应性

Sensitivity and reactivity to endothelin-1 in mesenteric beds and aortic rings of 4-week-old spontaneously hypertensive rats.

作者信息

Criscione L, Thomann H, Luu T D

机构信息

Cardiovascular Research Department, CIBA-GEIGY Ltd., Basle, Switzerland.

出版信息

Clin Exp Hypertens A. 1992;14(3):453-67. doi: 10.3109/10641969209036200.

Abstract

The vasoconstrictor effects of endothelin-1 were studied in perfused mesenteric vascular beds (MVB) and aortic rings of 4-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar Kyoto rats (WKY). Mean blood pressure (124 +/- 4 vs. 97 +/- 3 mmHg) and initial perfusion pressure in the MVBs (25 +/- 2 vs. 19.7 +/- 1.2) were significantly higher in SHR. Reactivity to endothelin-1 was increased in MVBs of SHR, as indicated by the maximum perfusion pressure obtained (223 +/- 8 vs 155 +/- 7 mmHg, p less than 0.001), whereas there was no significant difference in sensitivity between the two strains (EC50 values: 50 +/- 12 and 80 +/- 15 pmol, respectively). By contrast, in aortic rings reactivity and sensitivity to endothelin-1 were similar in both strains, (EC50s: 1.8 +/- 0.12 and 1.4 +/- 0.1 nM). Reactivity to norepinephrine was increased in MVBs, but reduced in aortic rings of SHR. The unchanged sensitivity to endothelin-1 and the unspecifically increased reactivity in the MVBs of SHR to endothelin-1 and norepinephrine indicate rather a change in vascular structure and not a functional abnormality. These results suggest that hyperreactivity to endothelin-1 may not be a primary hypertensive mechanism in genetic hypertension.

摘要

研究了内皮素 -1对4周龄自发性高血压大鼠(SHR)和年龄匹配的Wistar Kyoto大鼠(WKY)的灌注肠系膜血管床(MVB)和主动脉环的血管收缩作用。SHR的平均血压(124±4 vs. 97±3 mmHg)和MVB中的初始灌注压力(25±2 vs. 19.7±1.2)显著更高。如所获得的最大灌注压力所示(223±8 vs 155±7 mmHg,p <0.001),SHR的MVB对内皮素 -1的反应性增加,而两品系之间的敏感性无显著差异(EC50值分别为:50±12和80±15 pmol)。相比之下,在主动脉环中,两品系对内皮素 -1的反应性和敏感性相似(EC50分别为:1.8±0.12和1.4±0.1 nM)。SHR的MVB对去甲肾上腺素的反应性增加,但主动脉环中的反应性降低。SHR的MVB对内皮素 -1和去甲肾上腺素的敏感性不变以及非特异性增加的反应性表明血管结构发生了变化,而非功能异常。这些结果表明,对内皮素 -1的高反应性可能不是遗传性高血压的主要高血压机制。

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