title: Pharmacology of the steroid regulation of transmitter choice in cultured rat sympathetic ganglia.
abstract: The normally adrenergic rat superior cervical ganglion becomes cholinergic when grown in explant culture. This response is prevented by the physiological glucocorticosteroid, corticosterone, and the mineralocorticoid, aldosterone. The synthetic glucocorticosteroid, RU 26988, was also active in this respect. Progesterone, spironolactone, testosterone and 17 beta-estradiol were all inactive at 10(-6) M, demonstrating the specificity of the response. The response to 10(-7) M corticosterone was not antagonized by a hundred-fold excess of progesterone, testosterone, cortexolone or spironolactone. The response to 10(-7) M aldosterone was antagonized by spironolactone but not by progesterone. The order of potency of the agonists in this study is similar to that described for classical glucocorticoid receptors. The action of aldosterone was antagonized, however, by the mineralocorticoid antagonist, spironolactone. Thus, the steroid response described here may be mediated by both glucocorticoid and mineralocorticoid receptors or, alternatively, by a new glucocorticoid receptor which can be antagonized by a mineralocorticoid antagonist.
mesh_terms: D000450:Aldosterone / Q000494:pharmacology*; D000732:Androstanols / Q000494:pharmacology*; D000818:Animals; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003345:Corticosterone / Q000494:pharmacology*; D003350:Cortodoxone / Q000494:pharmacology; D005728:Ganglia, Sympathetic / Q000187:drug effects*; D011374:Progesterone / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013148:Spironolactone / Q000494:pharmacology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D000732:Androstanols; D013148:Spironolactone; D000450:Aldosterone; D011374:Progesterone; C038341:RU 26988; D014446:Tyrosine 3-Monooxygenase; D002795:Choline O-Acetyltransferase; D003345:Corticosterone; D003350:Cortodoxone