TY - JOUR
T1 - The dopamine receptors mediating inhibition of the sympathetic vasopressor outflow in pithed rats: pharmacological correlation with the D(2) -like type
AU - Manrique-Maldonado, Guadalupe
AU - Alcántara del Mercado Vázquez, Oscar
AU - Villamil Hernández, Ma. Trinidad
AU - González-Hernández, Abimael
AU - Marichal-Cancino, Bruno A.
AU - Centurión, David
AU - Villalón, Carlos M.
PY - 2011/8/8
Y1 - 2011/8/8
N2 - 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.
AB - 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.
KW - RAT
U2 - 10.1111/j.1742-7843.2011.00762.x
DO - 10.1111/j.1742-7843.2011.00762.x
M3 - Artículo
SN - 1742-7835
VL - 109
SP - 506
EP - 512
JO - Basic and Clinical Pharmacology and Toxicology
JF - Basic and Clinical Pharmacology and Toxicology
IS - 6
M1 - 109(6)
ER -