ACTH has a role in aldosterone synthesis and secretion, so ACTH deficiency could diminish serum aldosterone. However, to our knowledge, the effect of glucocorticoid administration and resultant suppression of ACTH secretion on serum aldosterone concentration has not been evaluated. The purpose of this study was to assess the effect of anti-inflammatory doses of prednisone administered over 4 weeks on aldosterone secretion in clinically healthy dogs.
Ten healthy adult American Fox Hounds were randomly assigned to placebo or prednisone (0.55 mg/kg PO q12h) groups. Serum sodium (Na), chloride (Cl), potassium (K) and bicarbonate (HCO3) concentrations were measured and ACTH stimulation tests were performed weekly beginning before (wk 0) and ending 2 weeks after cessation of drug administration (wk 6). For the stimulation test, ACTH (Cortrosyn) was administered (1.0 mcg/kg IV) and blood samples were taken before and at 20 and 60 min post. Aldosterone concentrations were measured in the pre and 20 min samples and cortisol in the pre and 60 min samples using previously validated radioimmunoassays. Repeated measures ANOVA on ranks was performed to assess changes over time within a group; significance was set at p<0.05.
For the treated dogs, compared to baseline, serum Na concentration at weeks 2-4 was significantly lower and at week 5 (i.e., one week after stopping the prednisone) significantly higher, serum Cl and corrected Cl concentrations at weeks 1-4 were significantly lower, and serum HCO3 concentration at weeks 2-4 was significantly higher. As expected, pre- and post-ACTH cortisol concentrations were significantly lower in dogs during prednisone therapy. Post-ACTH aldosterone concentrations were significantly lower than baseline on week 5.
Therefore, administration of anti-inflammatory doses of prednisone causes significant changes in clinically healthy dogs in serum Na, Cl, HCO3, cortisol and aldosterone concentrations. Although no change in aldosterone concentration was noted during glucocorticoid administration, interestingly, serum ACTH-stimulated aldosterone concentration decreases after cessation of glucocorticoid administration but quickly returns to normal.