This study was designed to investigate the long-term effects of
glucocorticoids on the control of mean arterial pressure (MAP) and renal function. Infusion of 10 mg/day of
methylprednisolone (MP), a
glucocorticoid with minimal
mineralocorticoid activity, for 10 days in six intact conscious dogs maintained on a
sodium intake of 78 mEq/day resulted in a decrease in MAP from 98 +/- 1 to 89 +/- 2 mm Hg, a decrease in
sodium iothalamate space to 89 +/- 2% of control, and a marked increase in glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and urinary
sodium excretion. Chronic infusion of MP at doses of 2--800 mg/day in four dogs maintained on low (5 mEq/day) or high
sodium intakes (160--223 mEq/day) also caused increases in GFR and ERPF, as well as natriuresis and decreased
sodium iothalamate space, while causing either no change or a slight reduction in MAP. To determine whether
glucocorticoids potentiate the chronic effects of
angiotensin II (AII) on MAP and renal function, MP was infused in dogs undergoing AII infusion (5 ng/kg/min). During AII
hypertension, chronic infusion of 5 or 10 mg/day of MP also resulted in a marked renal vasodilation, natriuresis, and reductions in
sodium iothalamate space, while causing small reductions in MAP. Thus, we found no evidence that chronic
glucocorticoid excess causes
hypertension in dogs, or that
glucocorticoids potentiate the blood pressure or renal effects of AII. Instead,
glucocorticoids tended to reduce MAP, probably because of chronic renal vasodilation, increased excretion of
sodium, and volume depletion.