ENDOTHELIN STIMULATED BY ANGIOTENSIN-II AUGMENTS CONTRACTILITY OF SPONTANEOUSLY HYPERTENSIVE RAT RESISTANCE ARTERIES
ENDOTHELIN STIMULATED BY ANGIOTENSIN-II AUGMENTS CONTRACTILITY OF SPONTANEOUSLY HYPERTENSIVE RAT RESISTANCE ARTERIES
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DOI：
10.1161/01.hyp.19.2.131
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发表时间：
1992-02-01
期刊：
影响因子：
8.3
通讯作者：
LUSCHER, TF
中科院分区：
文献类型：
--
作者：
DOHI, Y;HAHN, AWA;LUSCHER, TF
在培养的内皮细胞中，血管紧张素II刺激后产生内皮素。在离体大鼠肠系膜阻力动脉上观察血管紧张素II和内皮素-1对血管对去甲肾上腺素敏感性的影响。内皮素信使RNA（mRNA）的表达测定从肠系膜循环中获得的内皮细胞。血管紧张素II（10（-7）M）灌注动脉（5小时）可增强自发性高血压大鼠（但不包括Wistar-Kyoto大鼠）由去甲肾上腺素诱导的内皮动脉收缩。这种增强作用可被phosphoramidon和内皮素抗体抑制。血管紧张素II短期刺激（1小时）不会引起增强作用。用血管紧张素I刺激（10（-7）M; 5小时）引起增强作用，可被卡托普利阻止。从自发性高血压大鼠肠系膜动脉床收集的内皮细胞中，内皮素特异性mRNA组成型表达，血管紧张素II（10（-7）M）可增加内皮素转录物的水平。阈值浓度的外源性内皮素-1增强收缩诱导的去甲肾上腺素在动脉内皮和无自发性高血压大鼠，但不Wistar-Kyoto大鼠。因此，血管紧张素II刺激内皮细胞原位产生内皮素，从而增强自发性高血压大鼠肠系膜阻力动脉对去甲肾上腺素的收缩。这表明，血管内皮素的产生作为一个放大器的升压作用的肾素-血管紧张素系统，可能在高血压中发挥重要作用。
In cultured endothelial cells, endothelin is produced after stimulation with angiotensin II. The effects of angiotensin II and endothelin-1 on vascular sensitivity to norepinephrine were studied in perfused rat mesenteric resistance arteries. Expression of endothelin messenger RNA (mRNA) was determined in endothelial cells obtained from the mesenteric circulation. Perfusion (5 hours) of the arteries with angiotensin II (10(-7) M) potentiated contractions in arteries with endothelium induced by norepinephrine in spontaneously hypertensive rats but not Wistar-Kyoto rats. The potentiation was inhibited by phosphoramidon and an endothelin antibody. Short-term stimulation (1 hour) with angiotensin II did not cause the potentiation. Stimulation with angiotensin I (10(-7) M; 5 hours) caused a potentiation prevented by captopril. In endothelial cells collected from the mesenteric arterial bed of spontaneously hypertensive rats, endothelin-specific mRNA was constitutively expressed, and the level of endothelin transcripts was increased by angiotensin II (10(-7) M). Threshold concentrations of exogenous endothelin-1 potentiated contractions induced by norepinephrine in arteries with and without endothelium of spontaneously hypertensive rats but not Wistar-Kyoto rats. Thus, angiotensin II stimulates the endothelial production of endothelin in situ and thereby potentiates contractions to norepinephrine in mesenteric resistance arteries of spontaneously hypertensive rats. This suggests that vascular endothelin production acts as an amplifier of the pressor effects of the renin-angiotensin system that may play an important role in hypertension.