1. Plasma and urine free dopamine were measured daily for 5 days in six normal subjects maintained on a low sodium diet. The subjects were then given dietary supplements of sodium chloride for 5 days and the measurements repeated. 2. Throughout the experiment the 24 h free dopamine excretion rates for all the subjects were higher than could be accounted for by renal clearance. Dopamine excretion increased significantly in response to the added sodium chloride whereas plasma dopamine remained unchanged. The rise in dopamine excretion preceded that of sodium excretion. 3. It is concluded that free dopamine is formed within the kidney in response to increased dietary sodium and may have a role in the control of sodium excretion.

The effect of dietary sodium on the urine dopamine excretion of eight hypertensive patients and six matched controls was studied under metabolic balance conditions over a 2 week period during which dietary sodium intake was increased from 20 to 220 mmol/day. The control group showed the expected increase in dopamine excretion in response to sodium but the hypertensive patients showed an initial fall followed by a return to baseline values. Neither group showed a rise in blood pressure but the hypertensive patients showed a greater weight gain on salt loading, although this change was not significant. The cumulative sodium balance was greater and more prolonged in the hypertensive patients, although this difference also did not attain statistical significance. This defect in dopamine mobilization may be important in relation to renal sodium handling by patients with essential hypertension.

Glucose, fructose, sorbitol and myoinositol concentrations were measured in biopsies of peripheral nerve obtained at above-knee or below-knee amputation. In diabetic patients nerve glucose (median [range]) (5.09 [1.62-12.82] vs 3.12 [1.81-4.01]) p less than 0.001, fructose (0.245 [0.060-1.280] vs 0.150 [0.053-0.385]) p less than 0.05, and sorbitol (0.028 [0.012-0.496] vs 0.016 [0.007-0.059] p less than 0.02, mumol/g wet weight) were significantly higher than in non-diabetic patients. No significant difference was found in myoinositol concentration (1.95 [1.00-3.55] vs 2.09 [1.27-5.40] mumol/g wet weight). Concentrations differed markedly from previously reported values in human nerve obtained at post-mortem.

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Summary. Incubation in vitro of human red cells in increasing glucose concentrations results in a rise in both haemoglobin A1~ levels and an intermediate band when measured by an isoelectric focussing method. There are strong correlations between blood glucose levels, levels of haemoglobin Alc and the intermediate band both in vitro and in blood samples taken from diabetic patients. As the intermediate band is also included in the measurement of haemoglobin A~c by the usual analytical methods, this may lead to inaccurate results.

Aldose reductase has been shown to be present in both autonomic and somatic nerves. Activation of this enzyme and the polyol pathway has been demonstrated in diabetic animal models to cause a range of biochemical, functional, and structural consequences that include the accumulation of sorbitol and fructose; axoglial dysjunction; paranodal demyelination; abnormalities in axonal transport, blood flow, and vascular permeability; and resistance to ischemic transmission of action potentials. These data provide an insight into the range of processes that if activated may either singly or in combination result in altered patterns of nerve function and structural alterations in diabetic neuropathy. In animal models of diabetes, it has been shown that inhibition of aldose reductase can modify these diabetes-induced changes. It is hoped that the results of large-scale controlled trials will provide clinical evidence to support these data.

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