The dopamine receptors mediating inhibition of the sympathetic vasopressor outflow in pithed rats: Pharmacological correlation with the D 2-like type

Abstract

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 (25mg/kg) and desipramine (50μg/kg). The vasopressor responses to electrical stimulation of the sympathetic vasopressor outflow (0.03-3Hz; 50V and 2msec.) 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 (0.03-3μg/kg) was also investigated. Dopamine (3-100μg/kgmin.) inhibited the vasopressor responses to both electrical stimulation and noradrenaline. In contrast, SKF-38393 (10-100μg/kgmin.) failed to inhibit the vasopressor responses to electrical stimulation; whereas quinpirole (0.1-30μg/kgmin.) inhibited the vasopressor responses to electrical stimulation but not those to noradrenaline. The sympatho-inhibition by quinpirole (1μg/kgmin.) remained unaltered after i.v. SCH 23390 (300 and 1000μg/kg; D 1-like receptor antagonist), but was abolished after i.v. raclopride (1000μg/kg; D 2-like receptor antagonist). These doses of antagonists did not modify perse 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.