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The Dopamine Receptors Mediating Inhibition of the Sympathetic Vasopressor Outflow in Pithed Rats: Pharmacological Correlation with the D 2 ‐like Type
Author(s) -
ManriqueMaldonado Guadalupe,
GonzálezHernández Abimael,
MarichalCancino Bruno A.,
VillamilHernández Ma. Trinidad,
del Mercado Oscar AlcántaraVázquez,
Centurión David,
Villalón Carlos M.
Publication year - 2011
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2011.00762.x
Subject(s) - quinpirole , stimulation , endocrinology , medicine , sch 23390 , dopamine , raclopride , dopamine receptor , agonist , chemistry , pharmacology , receptor
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.