在清醒的正常血压大鼠中，依那普利拉可减弱内皮素-1诱导的肾血管收缩，而内皮舒张因子拮抗剂则可增强该作用。
Endothelin-1-induced renal vasoconstriction is blunted by enalaprilat and enhanced by EDRF antagonist in awake normotensive rats.
作者信息
Madeddu P, Anania V, Parpaglia P P, Troffa C, Pazzola A, Soro A, Manunta P, Tonolo G, Demontis M P, Varoni M V
机构信息
Clinica Medica and Farmacologia, University of Sassari, Italy.
出版信息
Clin Invest Med. 1991 Dec;14(6):600-6.
We attempt to elucidate the putative indirect mechanisms by which endothelin-1 affects mean blood pressure and renal blood flow in normotensive awake rats. Endothelin-1 (700 pg/kg, i.v.) induced a short-lasting decrease followed by a prolonged increase in mean blood pressure (from 113 +/- 4 to 92 +/- 4 mmHg at 30 sec, 132 +/- 7 mmHg at 10 min, and 129 +/- 6 mmHg at 30 min, p less than 0.01), and caused a profound and long-lasting fall in renal blood flow as measured by Doppler flowmeter technique (from 2.87 +/- 0.29 to 1.40 +/- 0.37 kHz at 30 sec, 1.77 +/- 0.32 kHz at 10 min and 2.10 +/- 0.45 kHz at 30 min, p less than 0.01). Neither the receptor antagonist of bradykinin D-Arg0-Hyp3-Thi5,8-DPhe7-bradykinin (30 micrograms/kg/min, i.v.) nor the antagonist of angiotensin II Sar1, Thr8-angiotensin II (4 micrograms/kg/min, i.v.) altered the changes in mean blood pressure and renal blood flow induced by endothelin-1. The antagonist of EDRF synthesis, NG-monomethyl-L-arginine (100 micrograms/kg/min, i.v.) enhanced the endothelin-1-induced increase in mean blood pressure (endothelin-1: 20 +/- 2 mmHg vs endothelin-1 + EDRF antagonist: 39 +/- 3 mmHg at 10 min, p less than 0.01) and decrease in renal blodo flow (endothelin-1: -40 +/- 4% vs endothelin-1 + EDRF antagonist: -73 +/- 3% at 10 min, p less than 0.01).2+ mediated by the blockade of angiotensin II formation.
我们试图阐明内皮素 -1影响正常血压清醒大鼠平均血压和肾血流量的假定间接机制。静脉注射内皮素 -1（700 pg/kg）可引起平均血压短暂下降，随后持续升高（30秒时从113±4 mmHg降至92±4 mmHg，10分钟时为132±7 mmHg，30分钟时为129±6 mmHg，p<0.01），并导致用多普勒流量计技术测量的肾血流量显著且持久下降（30秒时从2.87±0.29 kHz降至1.40±0.37 kHz，10分钟时为1.77±0.32 kHz，30分钟时为2.10±0.45 kHz，p<0.01）。缓激肽的受体拮抗剂D-Arg0-Hyp3-Thi5,8-DPhe7-缓激肽（30微克/千克/分钟，静脉注射）和血管紧张素II的拮抗剂Sar1, Thr8-血管紧张素II（4微克/千克/分钟，静脉注射）均未改变内皮素 -1诱导的平均血压和肾血流量变化。内皮舒张因子合成拮抗剂NG-单甲基-L-精氨酸（100微克/千克/分钟，静脉注射）增强了内皮素 -1诱导的平均血压升高（10分钟时，内皮素 -1组为20±2 mmHg，内皮素 -1+内皮舒张因子拮抗剂组为39±3 mmHg，p<0.01）以及肾血流量下降（10分钟时，内皮素 -1组为-40±4%，内皮素 -1+内皮舒张因子拮抗剂组为-73±3%，p<0.01）。由血管紧张素II形成受阻介导。 （注：原文最后一句表述似乎不完整且有拼写错误“2+ mediated by the blockade of angiotensin II formation”，译文按原样翻译）
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