Endogenous Regulation of the Pulmonary Response to Isoproterenol

Abstract

Pulmonary function was evaluated before and after isoproterenol administration in eight asthmatic patients who had been taking daily suppressive doses of glucocorticosteroids prior to study. Results were compared when the patients were not on glucocorticosteroid therapy, after glucocorticosteroid therapy, and after ACTH stimulation. Before isoproterenol administration, values were significantly closer to normal after ACTH than on no therapy or glucocorticosteroid therapy. Isoproterenol response was of great magnitude when no therapy was given and minimal after glucocorticosteroids or ACTH. Following isoproterenol, values were significantly closer to normal following ACTH compared to glucocorticosteroid therapy, and values on no therapy were intermediate not separating significantly from glucocorticosteroid therapy or ACTH stimulation. ACTH stimulates an increase in adrenal adenyl cyclase, cyclic AMP, and phenylethanolamine-N-methyl transferase with a resultant increase in the conversion of norepinephrine to epinephrine, a potent beta stimulator. The inability of these suppressed patients to release ACTH following discontinuation of glucocorticosteroids led to diminished epinephrine production, diminished endogenous beta stimulation, and maximal response to isoproterenol. Pulmonary function was evaluated before and after isoproterenol administration in eight asthmatic patients who had been taking daily suppressive doses of glucocorticosteroids prior to study. Results were compared when the patients were not on glucocorticosteroid therapy, after glucocorticosteroid therapy, and after ACTH stimulation. Before isoproterenol administration, values were significantly closer to normal after ACTH than on no therapy or glucocorticosteroid therapy. Isoproterenol response was of great magnitude when no therapy was given and minimal after glucocorticosteroids or ACTH. Following isoproterenol, values were significantly closer to normal following ACTH compared to glucocorticosteroid therapy, and values on no therapy were intermediate not separating significantly from glucocorticosteroid therapy or ACTH stimulation. ACTH stimulates an increase in adrenal adenyl cyclase, cyclic AMP, and phenylethanolamine-N-methyl transferase with a resultant increase in the conversion of norepinephrine to epinephrine, a potent beta stimulator. The inability of these suppressed patients to release ACTH following discontinuation of glucocorticosteroids led to diminished epinephrine production, diminished endogenous beta stimulation, and maximal response to isoproterenol.