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Dedeo?lu A, Fisher LA. 
“Central and peripheral injections of the 5-HT2 agonist, 1-2,5-dimethoxy-4-iodophenyl-2-aminopropane, modify cardiovascular function through different mechanisms”. 
J Pharmacol Exp Ther. 1991 Dec 07;259(3):1027-34.
The mechanisms underlying the cardiovascular effects of central and peripheral administration of the 5-HT2 serotonin receptor agonist -1-2,5-dimethoxy-4-iodophenyl-2-aminopropane hydrochloride DOI were studied in conscious rats. Intravenous 10-1000 nmol/kg and i.c.v. 3-300 nmol administration of DOI produced dose-related elevations of arterial pressure without altering heart rate except after injection of the highest doses. Pretreatment with xylamidine tosylate, a 5-HT2 receptor antagonist that does not cross the blood-brain barrier, blocked the pressor response to i.v., but not i.c.v., administration of equivalent doses of DOI. Pretreatment with the vasopressin receptor antagonist dCH25TyrMeAVP significantly reduced the pressor response to i.c.v., but not i.v., administration of DOI. Prior ganglionic blockade with chlorisondamine amplified the pressor response to both i.v. and i.c.v. administration of DOI. Pretreatment with a combination of chlorisondamine, xylamidine and dCH25TyrMeAVP abolished the pressor response to i.c.v. administration of DOI. Thus, the pressor response to i.v. administration of DOI was mediated at sites outside the blood-brain barrier, most likely at vascular 5-HT2 receptors, and was not secondary to vasopressin release. Inappropriate heart rate changes attended the pressor responses to i.v. administration of DOI, suggesting an action at extravascular sites. The pressor response to i.c.v. administration of DOI resulted from a combination of vasopressin release, modulation of autonomic nervous outflow and some leakage into the periphery.
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