PMID: 7932204Sep 1, 1994Paper

Central and peripheral mechanisms in the stimulation of adrenocortical secretion by the 5-hydroxytryptamine2 agonist, (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane

The Journal of Pharmacology and Experimental Therapeutics
J E Welch, D Saphier


The mechanisms by which the serotonin2A/2C (5-HT2A/2C) receptor agonist, (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) increase adrenocortical secretion were examined. Intraperitoneal (i.p., 2 mumol/kg) and intracerebroventricular (i.c.v., 0.1 pmol -40 nmol) administration of DOI increased plasma corticosterone (CS) concentrations. Administration of the 5-HT2A/2C antagonist, ketanserin (i.c.v.) also increased adrenocortical secretion, although the more selective 5-HT2A/2C antagonist, 6-methyl-1-(1-methylethyl)-ergoline-8 beta-carboxylic acid 2-hydroxy-1-methylpropyl ester (LY 53857) did not. In pentobarbital-anesthetized rats, DOI (i.c.v.) decreased adrenocortical secretion, whereas i.p. administration increased adrenocortical secretion. Ketanserin and LY 53857 (i.c.v.) failed to block CS responses after i.p. DOI, indicating that these increases were not principally due to central 5-HT2 receptor activation; only i.p. administration of ketanserin was able to block responses to DOI. Adrenocortical responses to DOI (i.p.) were preserved after lesions of the hypothalamic paraventricular nucleus or posterior hypothalamic deafferentations. However, responses to DOI were almost abolished in hypophysectomized animals, wherea...Continue Reading

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