The effect of sodium depletion and potassium loading on cortisol induced hypertension in sheep

Glucocorticoid induced hypertension has been regarded as independent of sodium (Na), in contrast to mineralocorticoid induced hypertension, which is Na+-dependent. These studies compare the effect of Na+ depletion and potassium (K+) loading on glucocorticoid hypertension induced by cortisol in conscious sheep. Cortisol (480 mg/d) for 5 days, in sheep on a normal chaff diet (90-140 mmol/d Na+, 200-250 mmol/d K+) increased mean arterial pressure by 18 mmHg on day 5, increased plasma Na+ concentration, reduced plasma K+ concentration, and did not change urinary Na+ excretion. Following Na+ depletion (Na+ loss 603 +/- 49 mmol), cortisol increased mean arterial pressure from 70 +/- 1 mmHg to 76 +/- 3 mmHg on day 5 (P less than 0.001) and the increase in pressure was significantly less than the increase seen on the normal diet (P less than 0.05). Plasma Na+ increased and plasma K+ decreased. Urinary Na+ and K+ excretion was unchanged. KCl loading (700-900 mmol/day) for 10 days had no effect on the maximum rise in mean arterial pressure (+18 mmHg with cortisol in K+ loaded sheep). Plasma Na+ and K+ fell, and urinary Na+ excretion increased during the infusion. These studies show that Na+ depletion, but not KCl loading, reduced cortisol induced hypertension in sheep. These data show that glucocorticoid hypertension is not independent of Na+ status.