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The serum corticosterone concentration in rats was increased by injection of quipazine, a relatively nonselective serotonin (5-hydroxytryptamine; 5-HT) agonist, or 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a serotonin agonist selective for the 5-HT^1A subtype of receptor. The quipazine-induced increase in serum corticosterone was antagonized by 17 different serotonin antagonists; of these, MDL 11939, pirenperone, setoperone, mianserin, LY 281067, ketanserin, ritanserin and clozapine have relatively selective affinity for the 5-HT₂ subtype of receptor. The 8-OH-DPAT-induced increase in serum corticosterone was not antagonized by metergohne, the most potent antagonist of the quipazine effect, but was antagonized by pindolol or penbutolol, 5-HTIA receptor antagonists. Pindolol did not block the effect of quipazine. The results support earlier evidence that serum corticosterone concentration in rats can be increased by activation of either 5-HT_1A or 5-HT₁ receptors. Indirect-acting serotonin agonists – fluoxetine, L-5-hydroxytryptophan and P^-chloroamphetamine – also increased serum corticosterone concentrations. The increases elicited by those agents, which earlier had been reported not to be blocked by metergohne pretreatment, also were not blocked by pretreatment with pindolol or with the combination of metergohne and pindolol. Thus, an involvement of a specific serotonin receptor subtype in the actions of these indirect agonists has not been established.