Impaired nitric oxide release by glomeruli from diabetic rats.
Basal nitric oxide (NO) production and NO responses to carbamylcholine (CCh) and the Ca2+ ionophore A23187 were measured with a NO electrode in glomeruli isolated from 2 to 3-month-diabetic versus age-matched control rats. In the presence of CCh or A23187, NO production was markedly reduced in glomeruli from diabetic versus control rats. Spontaneous generation of NO by s-nitrosopenicillamine (SNAP) was also reduced in the presence of glomeruli from diabetic rats as compared with values either in control glomeruli or in buffer alone. The results demonstrate an impairment of NO generation and/or stability in glomeruli from 2 to 3-month-diabetic rats, which correlates with the previously observed suppression of NO-dependent glomerular cyclic guanosine 3',5'-monophosphate (cGMP) induced by diabetes.
Craven
P A
PA
Department of Medicine, Veterans Affairs Medical Center, Pittsburgh, PA 15240, USA.
Studer
R K
RK
DeRubertis
F R
FR
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D005260:Female; D066298:In Vitro Techniques; D007678:Kidney Glomerulus / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D010396:Penicillamine / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D026423:S-Nitroso-N-Acetylpenicillamine
D009569:Nitric Oxide; D000001:Calcimycin; D026423:S-Nitroso-N-Acetylpenicillamine; D002217:Carbachol; D010396:Penicillamine