PRESSOR RESPONSIVENESS IN CORTICOSTEROID-INDUCED HYPERTENSION IN HUMANS

In previous studies short-term cortisol increased cold pressor responses and the rise in forearm vascular resistance accompanying intra-arterial norepinephrine without an increase in overall resting sympathetic nervous activity. The present study examined whether these alterations in pressor response are glucocorticoid or mineralocorticoid effects, or both. Normal male subjects (n=12) received either fludrocortisone, 0.3 mg daily (n=6), or dexamethasone, 3 mg daily (n=6), for 7 days. Hemodynamic studies were performed before and on day 7 of treatment. Fludrocortisone increased body weight from 69.3+/-1.8 to 71.1+/-2 kg (p<0.001), cardiac output from 5.0 to 6.0 l/min (+/-0.1, p<0.01), mean arterial pressure from 82+/-1 to 91+/-1 mm Hg (p<0.001), cold pressor responsiveness from 13.0 to 39.0 mm Hg/ml per 100 ml per minute (R units)(+/-0.3, p<0.01), and forearm vascular response to intra-arterial norepinephrine (F=59.4, p<0.01) and angiotensin II (F=30.8, p<0.01) infusions. Total peripheral resistance fell from 22.0 to 20.1 mm Hg/l per minute (+/-0.3, p<0.05). Dexamethasone did not increase cardiac output, 5.1 to 5.2 l/min (+/-0.1), or body weight but did increase mean arterial pressure from 82+/-3 to 91+/-3 mm Hg (p<0.001), cold pressor responsiveness from 8.6 to 17.1 R units (+/-2.8, p<0.05), and forearm vascular response to intra-arterial norepinephrine (F=33.0, p < 0.01) and angiotensin II (F= 54.9, p<0.01). Total peripheral resistance increased from 21.9 to 24.3 mm Hg/l per minute (+/-0.4, p<0.01). Thus, short-term fludrocortisone and dexamethasone produced similar rises in pressure: fludrocortisone with an increase in cardiac output and dexamethasone with an increase in resistance. Although hemodynamic patterns differ, increased pressor responsiveness is a feature of both mineralocorticoid and glucocorticoid administration in humans.