An alpha-adrenotropic study of the normal and diabetic rabbit kidney.
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.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D009638:Norepinephrine / Q000494:pharmacology*; D010477:Perfusion; D010646:Phentolamine / Q000494:pharmacology*; D011312:Pressure; D011433:Propranolol / Q000494:pharmacology; D011817:Rabbits; D011941:Receptors, Adrenergic / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*
D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D011433:Propranolol; D009638:Norepinephrine; D010646:Phentolamine