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链脲佐菌素诱导的糖尿病Wistar大鼠后肢对缓激肽血管舒张反应的选择性损伤

Selective impairment of hindquarters vasodilator responses to bradykinin in conscious Wistar rats with streptozotocin-induced diabetes mellitus.

作者信息

Kiff R J, Gardiner S M, Compton A M, Bennett T

机构信息

Department of Physiology and Pharmacology, Medical School, Queen's Medical Centre.

出版信息

Br J Pharmacol. 1991 Jun;103(2):1357-62. doi: 10.1111/j.1476-5381.1991.tb09793.x.

DOI:10.1111/j.1476-5381.1991.tb09793.x
PMID:1909198
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1908393/
Abstract
  1. Male, Wistar rats were treated with streptozotocin (STZ, 70 mg kg-1, i.p.) or saline and chronically instrumented with pulsed Doppler probes and intravascular catheters (implanted under sodium methohexitone anaesthesia) to allow assessment of haemodynamics in the conscious state 28 days later. 2. Control and STZ-treated rats received bolus doses of glyceryl trinitrate (10-80 nmol kg-1), acetylcholine (0.1-5 nmol kg-1) and bradykinin (0.3-30 nmol kg-1). 3. Although, as reported previously, STZ-treated rats had normal mean arterial blood pressure together with renal and mesenteric vasodilatations and hindquarters vasoconstriction relative to control rats, both groups showed similar hypotensive and regional haemodynamic responses to glyceryl trinitrate and acetylcholine. However, while the depressor effects of bradykinin were similar in control and STZ-treated rats, the former showed a hindquarters vasodilator response to bradykinin that was absent in the STZ-treated rats. 4. A loss of bradykinin-mediated vasodilatation in the hindquarters vascular bed in STZ-treated rats in the presence of normal, hindquarters vasodilator responses to other agents and normal bradykinin-mediated vasodilator responses in other vascular beds is consistent with existing evidence that the vasodilatation elicited by bradykinin in the hindquarters vascular bed is particularly dependent on nitric oxide synthesis and that this is impaired selectively in STZ-treated rats.
摘要
  1. 雄性Wistar大鼠接受链脲佐菌素(STZ,70 mg/kg,腹腔注射)或生理盐水处理,并长期植入脉冲多普勒探头和血管内导管(在甲己炔巴比妥钠麻醉下植入),以便在28天后评估清醒状态下的血流动力学。2. 对照组和STZ处理组大鼠接受硝酸甘油(10 - 80 nmol/kg)、乙酰胆碱(0.1 - 5 nmol/kg)和缓激肽(0.3 - 30 nmol/kg)的大剂量注射。3. 尽管如先前报道,与对照组大鼠相比,STZ处理组大鼠的平均动脉血压正常,同时肾和肠系膜血管舒张而后肢血管收缩,但两组对硝酸甘油和乙酰胆碱的降压及局部血流动力学反应相似。然而,虽然缓激肽对对照组和STZ处理组大鼠的降压作用相似,但前者对缓激肽表现出后肢血管舒张反应,而STZ处理组大鼠则没有。4. 在STZ处理组大鼠中,后肢血管床中缓激肽介导的血管舒张功能丧失,而对其他药物后肢血管舒张反应正常,且在其他血管床中缓激肽介导的血管舒张反应正常,这与现有证据一致,即缓激肽在后肢血管床中引起的血管舒张特别依赖于一氧化氮合成,而在STZ处理组大鼠中这种合成被选择性损害。

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Increased kidney size, glomerular filtration rate and renal plasma flow in short-term insulin-dependent diabetics.短期胰岛素依赖型糖尿病患者的肾脏大小、肾小球滤过率和肾血浆流量增加。
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