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Abstract
Rabbit kidneys from normal and alloxan-treated animals were isolated and perfused at 30 °C, with Krebs-Henseleit solution. Norepinephrine (NOR), 1 μg/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.