Exaggerated vascular response due to endothelial dysfunction and role of the renin-angiotensin system at early stage of renal hypertension in rats.

Exaggerated vascular response due to endothelial dysfunction and role of the renin-angiotensin system at early stage of renal hypertension in rats.
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大鼠肾性高血压早期由于内皮功能障碍和肾素-血管紧张素系统的作用而导致血管反应过度。

DOI:
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发表时间:
1994
影响因子:
20.1
通讯作者:
Z. Ono
Z. Ono
中科院分区:
医学1区
文献类型:
--
作者:
J. Hoshino;T. Sakamaki;T. Nakamura;M. Kobayashi;M. Kato;H. Sakamoto;T. Kurashina;A. Yagi;K. Sato;Z. Ono

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我们研究了内皮功能障碍是否可能导致大鼠单肾单夹肾性高血压(1K1C)早期给药去甲肾上腺素诱导的血管过度收缩。我们还研究了肾素血管紧张系统在这一现象中的作用。雄性Wistar大鼠在诱导肾动脉狭窄或假手术48 h后处死,获得胸主动脉环制备。用力-位移传感器分别记录去甲肾上腺素和乙酰胆碱作用下主动脉条的等距收缩和舒张。与对照组相比,1K1C大鼠主动脉对去甲肾上腺素的收缩反应明显(P < 0.05)增强。摩擦内皮和亚甲基蓝或ng -单甲基l -精氨酸醋酸酯处理能更大程度地增强对照大鼠对去甲肾上腺素的收缩反应;因此,各组的反应没有显著差异。第二个实验,大鼠在诱导肾动脉狭窄或假手术前1天、术后48小时,分别在饮用水中加入0.05%卡托普利、0.02%依那普利或0.02%尼卡地平。通过卡托普利或依那普利治疗,而尼卡地平治疗,1K1C大鼠主动脉对去甲肾上腺素的收缩反应增加,恢复到对照大鼠的水平。这些结果表明,内皮功能障碍可能导致1K1C大鼠去甲肾上腺素诱导的血管收缩过度,血管紧张素i转换酶抑制剂可以恢复内皮功能。
We investigated whether endothelial dysfunction might contribute to the exaggerated vasoconstriction that was induced by the administration of norepinephrine at the early stage of one-kidney, one-clip renal hypertension (1K1C) in rats. We also studied the role of the renin-angiotension system in this phenomenon. Male Wistar rats were killed 48 hours after the induction of renal artery stenosis or sham operation, and ring preparations of the thoracic aorta were obtained. The isometric contraction and relaxation of aortic strips produced by norepinephrine and acetylcholine, respectively, were recorded with a force-displacement transducer. The aorta of 1K1C rats showed a significantly (P < .05) exaggerated contractile response to norepinephrine as compared with that of control rats. Rubbing the endothelium and treatment with methylene blue or NG-monomethyl L-arginine acetate augmented the contractile responses to norepinephrine to a greater extent in control rats than in 1K1C rats; therefore, the responses of the groups did not differ significantly. In the second experiment, rats received 0.05% captopril, 0.02% enalapril, or 0.02% nicardipine in the drinking water for 1 day before and for 48 hours after the induction of renal artery stenosis or sham operation. The increased contractile responses of the aorta to norepinephrine in 1K1C rats were normalized to the level of the control rats by treatment with either captopril or enalapril but not with nicardipine. These results suggest that the endothelial dysfunction may contribute to the exaggerated norepinephrine-induced vasoconstriction observed in the 1K1C rats and that angiotensin I-converting enzyme inhibitors can restore the endothelial function.
在意识清醒的狗患高血压期间,α1-肾上腺素能血管敏感性增加。
DOI: 10.1152/ajpheart.1993.264.4.h1259
发表时间: 1993
期刊: The American journal of physiology
影响因子: --
作者:
Uemura,N;Vatner,DE;Shen,YT;Wang,J;Vatner,SF
通讯作者: Vatner,SF
DOI: --
发表时间: 1985-03
期刊: The Journal of pharmacology and experimental therapeutics
影响因子: --
作者:
W. Martin;G. Villani;D. Jothianandan;R. Furchgott
通讯作者: W. Martin;G. Villani;D. Jothianandan;R. Furchgott
DOI: 10.1161/01.res.57.5.781
发表时间: 1985-01-01
影响因子: 20.1
作者:
WEI, EP;KONTOS, HA;POVLISHOCK, JT
通讯作者: POVLISHOCK, JT
单肾、单夹肾高血压大鼠的微血管改变。
DOI: 10.1152/ajpheart.1984.246.5.h728
发表时间: 1984
期刊: The American journal of physiology
影响因子: --
作者:
Prewitt,RL;Chen,II;Dowell,RF
通讯作者: Dowell,RF
DOI: 10.1152/ajpheart.1986.250.5.h822
发表时间: 1986-05-01
影响因子: --
作者:
RUBANYI, GM;VANHOUTTE, PM
通讯作者: VANHOUTTE, PM