The central action of the 5‐HT 2 receptor agonist 1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI) on cardiac inotropy and vascular resistance in the anaesthetized cat

1 Experiments were carried out to determine the effects of the application of the selective 5‐HT 2 receptor agonist DOI intravenously (in the presence of the peripherally acting 5‐HT 2 receptor antagonist, BW501C67, 1 mg kg −1 , i.v.) or to the ‘glycine sensitive area’ of the ventral surface (30 μg each side) on the left ventricular inotropic (left ventricular d P /d t max) and vascularly isolated hindlimb responses in anaesthetized cats. For the ventral surface experiments, NMDA (10 μg each side) was applied to act as a positive control. In all experiments heart rate and mean arterial blood pressure were held constant to exclude any secondary effects caused by changes in these variables. 2 DOI ( n = 6 ) i.v or on the ventral surface had no effect on left ventricular d P /d t max but caused a significant increase in hindlimb perfusion pressure of 40±9 and 50±14 mmHg, respectively. Respiration was unaffected. NMDA ( n = 6 ), applied to the ventral surface, caused significant increases in both left ventricular d P /d t max and hindlimb perfusion pressure of 1950±349 mmHg s −1 and 69±17 mmHg respectively, with no associated change in left ventricular end‐diastolic pressure. The amplitude of respiratory movements increased. 3 It is concluded that activation of 5‐HT 2 receptors at the level of the rostral ventrolateral medulla (RVLM) excites sympathetic premotor neurons and/or their antecedents controlling hindlimb vascular resistance but not those controlling the inotropic effects on the left ventricle.British Journal of Pharmacology (1998) 125 , 1172–1179; doi: 10.1038/sj.bjp.0702183