Hydrocortisone-Induced Hypertension in Men

In previous studies we have shown that administration of 200 mg/day hydrocortisone (cortisol)to normal subjects raises blood pressure and cardiac output, with no change in total peripheral resistance or resting forearm vascular resistance. We have tested the hypothesis that this rise in cardiac output is essential for the rise in blood pressure (BP). Six normal volunteer men, aged 22 to 34 years, took part in two studies of 10 days, in random order, at least 4 weeks apart. Placebo (Study A) or 50 mg atenolol orally, 12 hourly (Study B), was given on days 1 to 10 and 50 mg Cortisol orally, 6 hourly, on days 5 to 10-. Blood pressure and cardiac output (Fick technique, alternative Doppler) were measured on days 4 and 10. In Study A (placebo and Cortisol) systolic BP rose from 116 to 125 mm Hg (standard error of the difference, SED 1.5), Ρ < .01, and in Study Β (atenolol and cortisol) from 109 to 120 mm Hg (SED 1.5), Ρ < ,01. Cardiac output (indirect Fick) rose from 4.8 ± 0.01 to 5.9 ± 0.2 L/m in , Ρ < .01, in A, and was unchanged in Study B, 4.4 ± 0.1 to 4.4 ± 0.2 L/min. Cardiac output measured by Doppler method was similar in pattern, 5.1 ± 0.2 to 6.7 ± 0.2 L/m in (P < .01) in A and 5.7 ± 0.2 to 5.8 ± 0.2 in B. Calculated peripheral resistance fell in Study A and increased in Study B. These data are consistent with the notion that the rise in blood pressure produced by cortisol administration in humans is not dependent on increase in cardiac output. Am J Hypertens 1993;6:287–294