1. In 29 patients with acromegaly, plasma renin activity and growth hormone were measured during fasting and recumbency on free diet. Exchangeable sodium was measured in all cases and expressed as a percentage of the expected value on the basis of lean body mass. 2. Twenty-two control subjects without evidence of cardiovascular, renal or endocrine disease were studied in the same way. 3. There was a significant increase in exchangeable sodium and suppression of plasma renin activity in the acromegalic patients in comparison with control subjects. 4. There was a significant positive correlation between exchangeable sodium and plasma growth hormone. 5. Hypertensive acromegalic patients (diastolic blood pressure larger than or equal to 100 mmHg) tend to have a lower (although not significantly so) exchangeable sodium than normotensive subjects. 6. We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly.

Administration of growth hormone-release inhibiting hormone (GH-RIH, somatostatin), as a 90 minute infusion (10 mug/min), to 3 healthy young men under conditons of active renin secretion acheived by pretreatment with furosemide (80 mg daily for 5 days), caused a mean 30% fall in plasma renin activity, which returned to basal levels immediately after stopping the GH-RIH infusion. Plasma aldosterone levels were not affected during the course of this experiment.

Summary Some chemical indices which could be related to diabetic complications have been assessed in 105 diabetics. In juvenile (insulin-dependent) diabetics with retinopathy, cardiovascular disease or nephropathy, levels of fibrinogen, fibrin monomer, beta-lipoprotein, cholesterol and alpha-2-macroglobulin were raised. Only in part is the explanation due to a rise of fibrinogen and cholesterol with age. Among twenty-six patients with a plasma fibrinogen over 400 mg/100 ml, eleven sustained a major cardiovascular catastrophe within the next 2 years. Alpha-1-acid-glycoprotein was raised in these eleven and beta-2-glycoprotein generally in juveniles with cardiovascular disease. Triglycerides were elevated in all groups, but notably in patients with Grade I retinopathy with venous dilation. There was a suggestion that triglycerides were related inversely to dietary carbohydrate in mature onset diabetics, and serum cholesterol in juveniles was related to insulin dosage. The part of lipids in vascular disease is then discussed. An interesting positive correlation was found between fibrin monomer, itself an indication of in vivo thrombin formation, and beta-lipoprotein. Although alpha-2-macroglobulin was elevated in juveniles, especially with complications, this did not apply to maturity onset cases and therefore no direct relation to diabetic vascular disease can be suggested. Moreover, alpha-2-macroglobulin levels were normal in acromegaly.

A study of patients on Kiil and Travenol coil dialysis has shown that kallikrein esterase, the kinin precursor, is increased in the venous blood during dialysis and that this is accompanied by an increase in the venous effluent of the dialysers. In addition Hageman factor depletion and an increase of platelet factor 4 has been found in the venous effluent. Such studies indicate surface activation of coagulation in the dialysers and will be of use in future studies of the suitability of different dialysers.

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