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Mediators and the effect of captopril on amino acid-induced hyperfiltration were studied. Acute intravenous L-arginine (arginine) infusion tests were performed twice, without captopril administration in 6 normal subjects (group I), before and after pretreatment with captopril in 10 normal subjects (group II) and 10 IgA nephropathy patients with slight renal dysfunction (group III). It was found that in all groups with and without captopril, arginine infusion led to a significant decrease in renal vascular resistance, and significant increases in renal plasma flow and plasma glucagon level. GFR was significantly increased in response to arginine only in normals without captopril pretreatment. Captopril pretreatment attenuated the rise in GFR following arginine infusion in normal subjects. Plasma renin activity and urinary cGMP were significantly increased in response to arginine only in normals without captopril pretreatment. No significant increase in urinary PGE2 was observed after arginine infusion in any groups. It was concluded that cGMP and glucagon are possible mediators for arginine-induced hyperfiltration and inhibition of renin-angiotensin system attenuates the arginine-induced rise in GFR.
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