This study investigated in pithed rats whether dopamine can inhibit the sympathetic vasopressor outflow and analysed the pharmacological profile of the receptors involved. Male Wistar pithed rats were pre-treated with intravenous (i.v.) bolus injections of gallamine (25 mg/kg) and desipramine (50 μg/kg). The vasopressor responses to electrical stimulation of the sympathetic vasopressor outflow (0.03-3 Hz; 50 V and 2 msec.) were analysed before and during i.v. continuous infusions of the agonists dopamine (endogenous ligand), SKF-38393 (D(1) -like) or quinpirole (D(2) -like). If inhibition was produced by any agonist, then its capability to inhibit the vasopressor responses to i.v. bolus injections of exogenous noradrenaline (0.03-3 μg/kg) was also investigated. Dopamine (3-100 μg/kg min.) inhibited the vasopressor responses to both electrical stimulation and noradrenaline. In contrast, SKF-38393 (10-100 μg/kg min.) failed to inhibit the vasopressor responses to electrical stimulation; whereas quinpirole (0.1-30 μg/kg min.) inhibited the vasopressor responses to electrical stimulation but not those to noradrenaline. The sympatho-inhibition by quinpirole (1 μg/kg min.) remained unaltered after i.v. SCH 23390 (300 and 1000 μg/kg; D(1) -like receptor antagonist), but was abolished after i.v. raclopride (1000 μg/kg; D(2) -like receptor antagonist). These doses of antagonists did not modify per se the sympathetically-induced vasopressor responses. In conclusion, quinpirole-induced inhibition of the sympathetic vasopressor outflow is primarily mediated by activation of dopamine D(2) -like receptors.
© 2011 CINVESTAV-IPN Basic & Clinical Pharmacology & Toxicology © 2011 Nordic Pharmacological Society.