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缓激肽对犬肾中升压激素血管效应的抑制作用:与前列腺素的关系。

Inhibition of bradykinin of the vascular effects of pressor hormones in the canine kidney: relationship to prostaglandins.

作者信息

Susić H, Nasjletti A, Malik K U

出版信息

Clin Sci (Lond). 1980 Dec;59 Suppl 6:145s-148s. doi: 10.1042/cs059145s.

Abstract
  1. Renal arterial injection of bolus doses of angiotensin II or noradrenaline, (0.06, 0.12 and 0.25 microgram) caused renal vasoconstriction and decreased blood flow to the kidney in a dose-related manner in dogs anaesthetized by sodium pentobarbital. 2. The effect of angiotensin II and noradrenaline in lowering renal blood flow was reduced during renal arterial infusion of either bradykinin (10 ng min-1 kg-1) or prostaglandin E2 (4 ng min-1 kg-1). 3. Pretreatment of the dogs with an inhibitor of prostaglandin synthesis, sodium meclofenamate (5 mg/kg), blunted the inhibitory action of bradykinin, but not that of prostaglandin E2, on renal vascular reactivity to angiotensin II and noradrenaline. 4. These results indicate that bradykinin reduces the renal vasoconstriction induced by angiotensin II and noradrenaline in the dog by a mechanism dependent upon synthesis of prostaglandins.
摘要
  1. 给戊巴比妥钠麻醉的犬肾动脉注射大剂量的血管紧张素II或去甲肾上腺素(0.06、0.12和0.25微克),可引起肾血管收缩,并使肾血流量呈剂量依赖性减少。2. 在肾动脉输注缓激肽(10纳克/分钟·千克-1)或前列腺素E2(4纳克/分钟·千克-1)期间,血管紧张素II和去甲肾上腺素降低肾血流量的作用减弱。3. 用前列腺素合成抑制剂甲氯芬那酸钠(5毫克/千克)预处理犬,可减弱缓激肽对肾血管对血管紧张素II和去甲肾上腺素反应性的抑制作用,但不影响前列腺素E2的抑制作用。4. 这些结果表明,缓激肽通过一种依赖于前列腺素合成的机制减轻犬体内血管紧张素II和去甲肾上腺素诱导的肾血管收缩。

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