Costa e Forti A, Fonteles M C
Arch Int Physiol Biochim. 1979 Dec;87(5):887-97. doi: 10.3109/13813457909070537.
Rabbit kidneys from normal and alloxan-treated animals were isolated and perfused at 30 degrees C, with Krebs-Henseleit solution. Norepinephrine (NOR), 1 microgram/min, promoted an increase in perfusion pressure which was blocked by phentolamine. In diabetic kidneys NOR induced a sluggish increase in perfusion pressure and resistance, showing a decrease in sensitivity of the adrenergic receptors to the drug. Propranolol, a beta-blocker, was able to elicit an alpha adrenergic blockade in diabetic kidneys. These facts demonstrate an adrenergic receptor defect in diabetic animals, which was shown just three weeks after alloxan treatment.
从正常和用四氧嘧啶处理过的动物体内分离出兔肾,并在30摄氏度下用克雷布斯-亨泽莱特溶液进行灌注。去甲肾上腺素(NOR),每分钟1微克,可使灌注压升高,这一作用可被酚妥拉明阻断。在糖尿病肾中,去甲肾上腺素引起的灌注压和阻力升高较为缓慢,表明肾上腺素能受体对该药物的敏感性降低。β受体阻滞剂普萘洛尔能够在糖尿病肾中引发α肾上腺素能阻断。这些事实证明糖尿病动物存在肾上腺素能受体缺陷,该缺陷在四氧嘧啶处理后仅三周就表现出来了。