1. Renal and cardiovascular effects of three dosages of insulin [50 (Ins I), 300 (Ins II) and 500 (Ins III) m-units h−1 kg−1] were investigated in healthy males by using a euglycaemic clamp technique. On separate days, control experiments were carried out to correct for any circadian variation in the variables studied.

2. All three insulin dosages resulted in a marked decline in fractional sodium excretion (actual experiments: basal, 0.95 ± 0.15%, Ins I, 0.79 ± 0.10%, Ins II, 0.80 ± 0.12%, Ins III, 0.84 ± 0.08%; control experiments: basal, 0.96 ± 0.10%, Ins I, 1.20 ± 0.12%, Ins II, 1.53 ± 0.15%, Ins III, 1.43 ± 0.10%; means ± sem, P < 0.005, analysis of variance). With the highest insulin dosage, the reduction in fractional sodium excretion tended to be less striking. This coincided with a rise in heart rate, pulse pressure and pulse rate-systolic blood pressure product (double product). Although blood pressure itself did not change, systolic blood pressure also tended to increase (actual experiments: basal, 133 ± 5 mmHg, Ins I, 132 ± 5 mmHg, Ins II, 139 ± 5 mmHg, Ins III, 143 ± 4 mmHg; control experiments: basal, 128 ± 3 mmHg, Ins I, 129 ± 3 mmHg, Ins II, 130 ± 3 mmHg, Ins III, 133 ± 3 mmHg; means ± sem, P = 0.09, analysis of variance). There was a positive correlation between the change in fractional sodium excretion and the change in systolic blood pressure over control values (r = 0.696, P < 0.028). At a rise in systolic blood pressure of 18 mmHg, the sodium-retaining effect of insulin appeared to be offset. A shift of the pressure-natriuresis relation to the right is suggested.

3. Plasma catecholamines did not change. Plasma renin activity increased from 1.11 ± 0.17 (basal) to 2.13 ± 0.31 (Ins III) pmol of angiotensin I h−1 ml−1; on the control day, a decline from 1.28 ± 0.24 (basal) to 0.81 ± 0.13 (Ins III) pmol of angiotensin I h−1 ml−1 was noted (P < 0.001). Despite this rise no concomitant rise in plasma aldosterone occurred.

4. Chronic hyperinsulinaemia may lead to blood pressure elevation in the long-term if it is postulated that resistance to the glucose-lowering effect of insulin is absent for the effects of insulin on the kidney and the cardiovascular system.

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