Regulation of Na(+)-pump activity by dopamine in rat tail arteries

We investigated the effect of dopamine on the vascular Na+-pump activity in isolated rat tail artery sections. Effect of dopamine on vascular tone was also assessed using a perfused tail artery preparation. Dopamine inhibited the Na+-pump activity in isolated rat tail arteries in a dose-dependent manner. Both SKF-38393 HCl, a selective dopamine D1 receptor agonist, and quinpirole HCl, a selective dopamine D2 receptor agonist inhibited the Na+-pump activity. The inhibition of the Na+-pump activity. The inhibition of the Na+-pump by dopamine was accompanied with a transient increase in the vascular tone. SKF-38393, but not quinpirole produced a sustained increase in the vascular tone. Tissues preincubated simultaneously with SCH-23390 HCl, a selective dopamine D1 receptor antagonist, and sulpiride, a selective dopamine D2 receptor antagonist, prevented the dopamine inhibition of the Na+-pump activity. Pertussis toxin blocked the Na+-pump inhibition produced by the dopamine D1 receptor agonist but not by the dopamine D2 agonist. Similarly, the dopamine D1 receptor but not dopamine D2 agonist increased the rate of phosphoinositide hydrolysis in rat tail artery sections. Our results indicate that dopamine inhibition of the Na+-pump is mediated by a pertussis toxin-sensitive mechanism and may be coupled to the activation of the phospholipase C system in rat tail arteries. The modulation of the Na+-pump by dopamine may contribute to the vascular tone.