摘要
Objective To investigate the nitric oxide (NO) dependent 3′, 5′ cyclic guanosine monophosphate (cGMP) stimulation or inhibition in isolated glomeruli and inner medullary collecting duct(IMCD) cells from normal and diabetic rats for elucidating the probable role of NO in diabetic nephropathy. Methods Glomeruli and IMCD cells were obtained from anesthetized diabetic rats , 2 weeks after streptozotocin induction, and normal rats, and incubated for 10 minutes under basal state or adding different drugs. cGMP was measured by radioimmunoassay. Results Diabetic glomeruli had a higher generation of cGMP under basal state but failed to further response to L arginine, which was contrary to the glomeruli from normal rats. NG monomethyl L arginine prevented the elevation of cGMP after L arginine stimulation in normal rats but not in diabetic rats. Acetylcholine produced a concentration dependent of cGMP accumulation in the glomeruli of both groups, but the extent was relatively smaller in diabetic than in normal. A similar tendency was also observed in sodium nitroprusside treated glomeruli. However the cGMP increment in response to atrial natriuretic peptide was identical in the two groups. For the IMCD cells, neither the difference of basal cGMP nor those responses related to acetylcholine or sodium nitroprusside could be observed. But the attenuated response to L arginine also existed in diabetic IMCD cells. Conclusion Both diabetic glomeruli and IMCD cells have an abnormal NO metabolism, which may account in part for the disturbance of renal hemodynamics.
Objective To investigate the nitric oxide (NO) dependent 3′, 5′ cyclic guanosine monophosphate (cGMP) stimulation or inhibition in isolated glomeruli and inner medullary collecting duct(IMCD) cells from normal and diabetic rats for elucidating the probable role of NO in diabetic nephropathy. Methods Glomeruli and IMCD cells were obtained from anesthetized diabetic rats , 2 weeks after streptozotocin induction, and normal rats, and incubated for 10 minutes under basal state or adding different drugs. cGMP was measured by radioimmunoassay. Results Diabetic glomeruli had a higher generation of cGMP under basal state but failed to further response to L arginine, which was contrary to the glomeruli from normal rats. NG monomethyl L arginine prevented the elevation of cGMP after L arginine stimulation in normal rats but not in diabetic rats. Acetylcholine produced a concentration dependent of cGMP accumulation in the glomeruli of both groups, but the extent was relatively smaller in diabetic than in normal. A similar tendency was also observed in sodium nitroprusside treated glomeruli. However the cGMP increment in response to atrial natriuretic peptide was identical in the two groups. For the IMCD cells, neither the difference of basal cGMP nor those responses related to acetylcholine or sodium nitroprusside could be observed. But the attenuated response to L arginine also existed in diabetic IMCD cells. Conclusion Both diabetic glomeruli and IMCD cells have an abnormal NO metabolism, which may account in part for the disturbance of renal hemodynamics.
