Exp Clin Endocrinol Diabetes 1985; 85(2): 217-222
DOI: 10.1055/s-0029-1210439
Original

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

The Effect of Long-Term Verapamil Treatment on the Secretion of Cortisol and Aldosterone in Subjects with Normal and High Blood Pressure

I. Žofková
  • Research Institute of Endocrinology (Director: MUDr. RNDr. L. Starka, DrSc), Prague/Czechoslovakia
Further Information

Publication History

1984

Publication Date:
16 July 2009 (online)

Summary

Based on their previous observations of the stimulating action of verapamil on the secretory reserve of cortisol after one-week oral administration to healthy volunteers, the author investigated the effect of this calcium entry blocker on the adrenocortical function (cortisol and aldosterone secretion) during therapeutic administration to patients with mild arterial hypertension and normotensive patients suffering from Raynaud's syndrome. Verapamil, 3—4x80mg per day by the oral route, did not lead to significant changes of cortisol levels at rest nor after ACTH stimulation when assessed at the end of the first month of treatment in both groups. However, normotensive subjects with Raynaud's syndrome showed a decline of ACTH stimulated cortisolaemia during the 3rd month (p < 0.05) and 4th month (p < 0.01) and a reduction of cortisol secretory reserve (Δcortisol) during the 3rd month of treatment (p < 0.05). In aldosterone secretion of normotensives with Raynaud's syndrome no significant changes were observed. In hypertensive subjects, the decline of ACTH stimulated cortisolaemia at the end of the 3rd and 4th month was not significant and Δ cortisol did not change. The initial aldosterone levels before and after ACTH and Δ aldosterone before treatment of hypertensives was lower as compared with normotensives (p < 0.01, p < 0.01 and p < 0.05, respectively), and increased gradually during treatment in the 4th month significantly (p < 0.05, p < 0.01 and p < 0.01, respectively). The hypotensive effect of verapamil persisted throughout the treatment. It is suggested, that after initial nonspecific adrenocortical stimulation the calcium entry blocking effect of verapamil is manifested after more prolonged treatment by inhibition of stimulated cortisolaemia. Aldosterone stimulating effect of verapamil in hypertensives is on the other hand most propably a nonspecific effect which awaits confirmation. The exact mechanism of described hormonal changes remains to be determined in future