Impaired nitric oxide release by glomeruli from diabetic rats

PA Craven, RK Studer, FR DeRubertis - Metabolism, 1995 - Elsevier
PA Craven, RK Studer, FR DeRubertis
Metabolism, 1995Elsevier
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 …
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.
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