Metabolism - Clinical and Experimental
Volume 44, Issue 6 , Pages 695-698, June 1995

Impaired nitric oxide release by glomeruli from diabetic rats☆

Department of Medicine, Veterans Affairs Medical Center and University of Pittsburgh, Pittsburgh, PA, USA

Received 30 June 1994; accepted 6 December 1994.

Abstract 

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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☆ Supported by the General Medical Research Service of the Department of Veterans Affairs and a grant from the Juvenile Diabetes Foundation.

PII: 0026-0495(95)90178-7

Metabolism - Clinical and Experimental
Volume 44, Issue 6 , Pages 695-698, June 1995

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