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Muscle sympathetic vasoconstrictor activity in hydrocortisone-induced hypertension in humans
V G Macefield1, P M Williamson, L R Wilson
1Prince of Wales Medical Research Institute, Randwick, Australia.
Aim:
This study was undertaken to test the hypothesis that increased sympathetic vasomotor drive is responsible for cortisol-induced hypertension.
Methods:
Ten healthy male subjects on a fixed sodium diet (150 mmol/day) were randomized to five days of treatment with cortisol (200 mg/day) or placebo in a double-blind crossover study. On day 5 of each treatment, multi-unit muscle sympathetic activity was recorded from the common peroneal nerve. Resting muscle sympathetic activity (MSA) was measured in the recumbent position and stimulated MSA was measured in the final 20 sec of end-inspiratory capacity apnoea and end-expiratory apnoea and in the second minute of a cold pressor stimulus. A subgroup of six subjects also underwent identical MSA measurements following 5 days treatment with dexamethasone (3 mg/day).
Major Findings:
Cortisol, but not placebo, significantly increased systolic (115+/-2 vs 129+/-3 mmHg precortisol vs cortisol day 5, p < 0.001) and diastolic blood pressure (53+/-3 vs 61+/-3, p < 0.05). Resting MSA was significantly reduced by cortisol (23.9+/-2.3 to 5.0+/-2.0 bursts/min, placebo vs cortisol, p < 0.01). Cortisol significantly attenuated the increase in MSA observed at end-inspiratory apnoea (56.3+/-3.9 vs 35.4+/-6.6, p < 0.05) and end-expiratory apnoea (50.5+/-3.5 vs 26.3+/-6.2 bursts/min, n = 8, p < 0.05), and during the cold pressor response (55.0+/-12.7 vs 21.4+/-7.6, n = 5, p < 0.05). Dexamethasone significantly increased systolic blood pressure and suppressed resting and stimulated MSA. No changes in body weight, haematocrit or angiotensin II concentrations occurred during dexamethasone treatment.
Conclusion:
MSA is significantly suppressed by cortisol treatment. As suppression of MSA is also observed during treatment with the pure glucocorticoid dexamethasone, suppressed MSA cannot be attributed to increased plasma volume or to changes in angiotensin II concentration. We conclude that cortisol-induced hypertension is not due to increased muscle sympathetic vasomotor drive.