Role of mineralocorticoids and glucocorticoids in blood pressure regulation in normotensive rats

The separate role of mineralocorticoid and glucocorticoid hormone action in maintaining arterial pressure was studied in normotensive rats. Four groups were prepared: adrenalectomized (ADX) rats given 6 μg aldosterone/24 h (ALDO; n = 9) or 10 μg dexamethasone/24 h (DEX; n = 9) by intraperitoneal Alzet pumps, sham-operated controls (control; n = 10) and ADX rats with no hormone replacement (ADX; n = 9). All groups were given 1% NaCl + 2.5% glucose drinking solution. Measurements of plasma corticosterone and aldosterone and urinary aldosterone excretion confirmed the adequacy of the experimental groups. Forty-eight hours after ADX or sham, base-line intra-arterial mean arterial pressure (MAP) in conscious undisturbed rats was similar in the four groups. Captopril (1 mg/kg iv) produced a similar reduction in MAP in ALDO (-11 ± 2 mmHg) and DEX (-12 ± 1 mmHg) groups, despite a lower plasma renin activity (PRA) in ALDO (2.0 ± 0.7 and 6.0 ± 1.5 ng·ml^-1·h^-1, respectively; P < 0.05). dP(Me)TyrAVP (50 μg/kg/iv) caused a greater decrease in MAP in ALDO (-15 ± 3 mmHg) than in DEX (-8 ± 1 mmHg; P < 0.05). Combined blockade with both antagonists resulted in a greater MAP reduction in ALDO (-29 ± 4 mmHg) than in DEX (-15 ± 4 mmHg; P < 0.05). These results indicate that glucocorticoid hormone action maintains arterial pressure in ADX rats by mechanisms similar to normal rats and largely independent of the renin-angiotensin system and vasopressin. In contrast, mineralcorticoid replacement alone in ADX rats requires increased participation of both peptide systems for maintenance of arterial pressure.