Glucose and insulin exert additive ocular and renal vasodilator effects onhealthy humans

Aims/hypothesis. There is evidence that insulin and glucose cause renal and ocular vasodilation, There is, however, currently no data on the effect of combined hyperglycaemia and hyperinsulinaemia on the renal and ocular bloo d flow seen in diabetic patients on insulin therapy. Methods. We carried out two different 3-way crossover studies in healthy su bjects (each, n = 9). In study one, hyperglycaemic clamps (5.6 mmol/l, 11.1 mmol/l, 16.7 mmol/l) were carried out during placebo or insulin (dose 1:1 mU/kg/min; dose 2: 2 mU/kg/min) infusion. The second study was identical bu t endogenous insulin secretion was blocked with somatostatin. The renal pla sma flow, glomerular filtration rate and pulsatile choroidal blood flow wer e measured using the paraaminohippurate method, the inulin method and a las er interferometric measurement of fundus pulsation amplitude, respectively. Results. Insulin increased renal plasma flow and fundus pulsation amplitude but not the glomerular filtration rate. Hyperglycaemia increased all the r enal and ocular parameters studied. Haemodynamic effects of glucose and ins ulin were additive when somatostatin was co-administered but not under basa l conditions. Conclusions/interpreration. Glucose and insulin can exert additive vasodila tor properties on renal and ocular circulation. To find out whether this ob servation is related to the increased regional perfusion in diabetes longit udinal studies on patients with Type I (insulin-dependent) diabetes mellitu s are needed.