Blood Pressure and Metabolic Effects of Cortisol and Deoxycorticosterone in Man

Abstract

We have previously shown that ACTH administration (1 mg/day) for 5 days raises systolic blood pressure (BP) by some 20 mmHg in both normotensive and hypertensive subjects, accompanied by hypokalaemia, urinary Na retention, a rise in fasting blood glucose and a fall in plasma renin concentration (PRC). In the present study cortisol and deoxycorticosterone (DOC) were infused for 5 days in 7 and 6 subjects respectively at rates appropriate for conditions of ACTH stimulation to determine whether the effects of ACTH could be reproduced by either steroid. Cortisol infusion increased systolic BP from a control of 108 ± 7 mmHg to 129 ± 7 mmHg on day 5, p < 0.001. Plasma [Na] increased from 137 ± 1 to 139 ± 1 mmol/1 (p < 0.01), plasma [K] fell from 3.8 ± 0.1 to 3.6 ± 0.1 mmol/1 (p < 0.05); blood glucose rose from 3.9 ± 0.2 to 4.7 ± 0.2 mmol/1 (p < 0.001); PRC fell from 26 ± 7 to 12 ± 3 μiu/ml (p < 0.05); renin substrate rose from 1629 ± 140 to 2206 ± 453 pmol AI/ml, (p < 0.05); urine Na excretion fell from 93 ± 19 to 41 ± 10 mmol on day 2 (p < 0.05) and rose to 209 ± 31 mmol 48 hrs after infusion (p < 0.001); urine output rose from 2.0 ± 0.35 to 2.89 ± 0.46 L on day 5, (p < 0.01). Plasma cortisol levels were similar to those seen with ACTH treatment. DOC infusion was associated with a fall in diastolic BP (control 64.2 ± 4.0 mmHg, day 5 57.0 ± 4.2 mmHg, p < 0.01). Urine Na excretion fell from 77 ± 1 2 mmol/day to 49 ± 8 mmol/day on day 1, (p=0.06) and body weight rose from 76.0 ± 5.8 kg to 76.8 ± 5.9 kg day 5 (p < 0.001). Thus in man, cortisol infusion (in contrast to DOC) at rates appropriate for conditions of ACTH stimulation reproduces both the BP and metabolic effects of ACTH. Whether cortisol acts to raise blood pressure by a classical glucocorticoid mechanism or by a hypertensinogenic mechanism is not known.

Key Words:

• ACTH
• Blood Pressure
• Cortisol
• Deoxycorticosterone
• Electrolytes
• Man
• Renin