Urinary dopamine response to angiotensin II is not abnormal in type 1 (insulin-dependent) diabetes mellitus

To examine the interaction between angiotensin II (ANGII) anddopamine in type I diabetes mellitus, urinary dopamine excretionwas examined during ANGII infusion in 15 diabetic patients and10 control subjects after pretreatment with lithium 750 mg andplacebo. The antinatriuretic response and the urinary dopamineresponse to ANGII did not differ within or between the two groupson each study day. No correlation was observed between the decrementsin urinary sodium excretion and urinary dopamine output duringANGII infusion in either group. The effect of insulin on urinarydopamine excretion was studied separately in seven non-diabeticsubjects; sodium and potassium retention occurred during a hyperinsulinaemiceuglycaemic clamp, but urinary dopamine did not change. Thedata suggest that the relationship between urinary sodium excretionand tubular dopamine synthesis remains normal in early type1 diabetes mellitus both at baseline and during the antinatriuresisinduced by angiotensin II. The cause of the reduction in urinarydopamine during ANGII infusion is unclear, but is probably notmediated directly by changes in proximal tubular sodium transport.