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In elderly patients diabetes and hypertension play an important and synergistic role in the development of cardiovascular complications. For this reason therapy must reduce blood pressure without compromising blood glucose control. We investigated the question of whether captopril, an angiotensin converting enzyme inhibitor, can be used without interference to glucose metabolism in diabetics with secondary failure. Ten elderly hypertensive diabetics (diastolic blood pressure greater than 95 mmHg), maintained in good metabolic control using oral hypoglycaemic agents and insulin, were studied before and after 30 days of captopril at 100 mg/day. We measured the following parameters: blood pressure, heart rate, fructosamine and a daily profile for blood glucose and c-peptide. There was a statistically significant reduction in systolic and diastolic blood pressure. No difference was observed in the levels of blood glucose and fructosamine. Insulin secretion as determined by c-peptide levels was not modified, in contrast with findings reported for the use of beta-blockers, diuretics or nifedipine. It seems that captopril is useful and without side effects, even in secondary-failure diabetic patients characterized by unstable metabolic control.

The influence of combined therapy using insulin and oral hypoglycaemic agents on blood glucose control and on insulin secretion in Type 2 diabetic patients with secondary failure to oral hypoglycaemic agents was evaluated. Type 2 diabetic patients (n = 180) (98 normal-weight, 82 over-weight), at least 3 years from diagnosis, and having poor blood glucose control on oral hypoglycaemic agents for at least 3 months (fasting plasma glucose greater than 10.0 mmol l-1) despite intensive efforts at improvement, were included in the study. A single daily insulin injection (human ultralente), at a dose of 0.22 +/- 0.07 U kg-1 d-1 in normal-weight and 0.33 +/- 0.10 U kg-1 d-1 in over-weight patients, was added to the previous dietary and drug treatment for 6 months. A progressive and significant (2p less than 0.001) reduction of the mean daily blood glucose was observed during the first 3 months of combined therapy (from 13.2 +/- 3.2 to 8.1 +/- 2.1 mmol l-1 in normal-weight and from 13.4 +/- 3.1 to 8.8 +/- 2.3 mmol l-1 in over-weight patients), with no further significant changes thereafter. A significant increase (2p less than 0.001) in the mean daily C-peptide concentration (from 0.50 +/- 0.30 to 0.71 +/- 0.29 nmol l-1 in normal-weight and from 0.78 +/- 0.36 to 1.00 +/- 0.41 nmol l-1 in over-weight patients) took place during combined therapy. No changes of body weight (+ 1.5 +/- 1.2 kg in normal-weight and + 1.0 +/- 1.0 kg in over-weight patients) were observed.

The aim of this study is to contribute to the understanding of the probable role of the renin-angiotensin-aldosterone, the kallikrein-kinins and the prostaglandins systems on the various types of essential hypertension and also their contribution to the action of captopril. Nineteen patients, 7 with high and 12 with normal or low levels of plasma renin activity (PRA), have been studied. Captopril (100 mg) was administered in acute dosage, blood pressure was checked for two hours and PRA and plasma aldosterone were assayed. The same trial was repeated after inhibition of prostaglandin-synthetase with indomethacin and kallikrein with trasylol, alternatively, and then with indomethacin and trasylol, contemporaneously. Our results showed that the renal vasodilative system was probably also involved in the mechanism of action of captopril, but that this drug reduced blood pressure mainly through a block of angiotensin II production in both groups of patients. Thus the finding of a normal or low PRA does not justify the conclusion that angiotensin II is not one of the mechanisms responsible for an elevated arterial pressure.