PT  - JOURNAL ARTICLE
AU  - Lin, M T
TI  - Effects of brain serotonin alterations on prostaglandin E1-induced bradycardia in rats.
DP  - 1979 Feb 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 232--235
VI  - 208
IP  - 2
4099  - http://jpet.aspetjournals.org/content/208/2/232.short
4100  - http://jpet.aspetjournals.org/content/208/2/232.full
SO  - J Pharmacol Exp Ther1979 Feb 01; 208
AB  - The vasodepressor and bradycardia responses of saline control, serotonin-depleted and serotonin-potentiated rats to an intravenous dose of prostaglandin E1 (PGE1) were assessed under the urethane anesthesia. Elevation of serotonin concentration in brain with either 5-hydroxytryptophan (a serotonin precursor) or chlorimipramine (an inhibitor of serotonin reuptake), although causing no changes in vasodepressor reuptake), although causing no changes in vasodepressor response, did enhance the PGE1-induced bradycardia in contrast, depleting serotonin concentration in brain with either p-chlorophenylalanine or 5,7-dihydroxytryptamine greatly reduced the PGE1-induced bradycardia without changes in vasodepressor response. Moreover, the reduced PGE1 bradycardia induced by p-chlorophenylalanine treatment was readily reversed by the replacement of the depleted brain serotonin with 5-hydroxytryptophan in combination with a peripheral decarboxylase inhibitor Ro4-4602. The data indicate that brain serotonergic systems play a role in the elaboration or modulation of the PGE1-induced bradycardia. Specifically, brain serotonin seems to facilitate the PGE1-induced bradycardia since its depletion causes a decrease and its potentiation or elevation causes an increase in the PGE1-induced bradycardia.