Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Deleg. Tlalpan, 14330, Mexico DF, Mexico.
Naunyn Schmiedebergs Arch Pharmacol. 2013 May;386(5):393-403. doi: 10.1007/s00210-013-0841-8. Epub 2013 Feb 19.
We have recently reported that quinpirole (a D2-like receptor agonist) inhibits the vasopressor sympathetic outflow in pithed rats via sympatho-inhibitory D2-like receptors. Since D2-like receptors consist of D2, D3 and D4 receptor subtypes, this study investigated whether these subtypes are involved in the above quinpirole-induced sympatho-inhibition by using antagonists of these receptor subtypes. One hundred fifty-six male Wistar rats were pithed and prepared for preganglionic spinal (T7-T9) stimulation of the vasopressor sympathetic outflow. This approach resulted in frequency-dependent vasopressor responses which were analysed before and during i.v. continuous infusions of either saline (0.02 ml/min) or quinpirole (1 μg/kg.min) in animals receiving i.v. bolus injections of vehicle [saline or dimethyl sulfoxide (DMSO)] or the antagonists L-741,626 (D2), nafadotride or SB-277011-A (both D3) as well as L-745,870 (D4). Quinpirole inhibited the sympathetically-induced vasopressor responses. This sympatho-inhibition was (a) unaltered after 1 ml/kg saline, DMSO or 100 and 300 μg/kg L-741,626; (b) markedly blocked and abolished by, respectively, 30 and 100 μg/kg nafadotride or 100 and 300 μg/kg SB-277011-A and (c) slightly blocked after 30 and 100 μg/kg L-745,870, but 300 μg/kg L-745,870 produced no blockade whatsoever. Except for 300 μg/kg L-741,626 or 300 μg/kg L-745,870, the doses of the above compounds failed to modify per se the sympathetic vasopressor responses. The inhibition of the vasopressor sympathetic outflow induced by 1 μg/kg.min quinpirole in pithed rats is predominantly mediated by dopamine D3 and, to a lesser extent, by D4 receptor subtypes, with no evidence for the involvement of the D2 subtype.
我们最近报道,喹吡罗(一种 D2 样受体激动剂)通过抑制性 D2 样受体抑制去甲酰化的大鼠的升压交感传出。由于 D2 样受体包括 D2、D3 和 D4 受体亚型,因此本研究使用这些受体亚型的拮抗剂研究了这些亚型是否参与了上述喹吡罗诱导的交感抑制作用。156 只雄性 Wistar 大鼠被去甲酰化并准备进行节前脊髓(T7-T9)刺激升压交感传出。这种方法导致了频率依赖性的升压反应,在动物接受静脉推注载体[盐水或二甲亚砜(DMSO)]或拮抗剂 L-741,626(D2)、nafadotride 或 SB-277011-A(均为 D3)以及 L-745,870(D4)的静脉连续输注期间,对这些反应进行了分析。喹吡罗抑制了交感神经引起的升压反应。这种交感抑制作用:(a)在 1ml/kg 盐水、DMSO 或 100 和 300μg/kg L-741,626 后未改变;(b)分别被 30 和 100μg/kg nafadotride 或 100 和 300μg/kg SB-277011-A 显著阻断和消除;(c)在 30 和 100μg/kg L-745,870 后略有阻断,但 300μg/kg L-745,870 则无阻断作用。除了 300μg/kg L-741,626 或 300μg/kg L-745,870 之外,上述化合物的剂量本身均未改变交感升压反应。在去甲酰化的大鼠中,1μg/kg.min 喹吡罗诱导的升压交感传出抑制主要由多巴胺 D3 介导,其次是 D4 受体亚型,而没有证据表明 D2 受体亚型参与。