title: Dopamine constricts porcine pial veins.
abstract: Dopamine has been shown to induce pial arterial relaxation and constriction in several species. Its mode of action on pial veins, however, remains unclarified. The vasomotor effect of dopamine on porcine pial veins was, therefore, examined using an in vitro tissue bath technique. The results indicated that dopamine constricted exclusively isolated ring segments of pial veins in the presence or absence of active muscle tone. The constriction induced by dopamine was not affected by N(omega)-nitro-L-arginine (L-NNA, 2 x 10(-5) M) or indomethacin (10(-5) M). Only in few preparations was the constriction induced by maximum concentration of dopamine potentiated by L-NNA, suggesting that dopamine at high concentrations may release NO or a NO-related substance. In the presence of L-NNA (2 x 10(-5) M), dopamine-induced constriction was inhibited by phentolamine and yohimbine (but not prazosin) in a concentration-dependent manner with maximum inhibition at 10(-6) M. SKF38393 and 6-bromo-APB (selective dopamine D1 receptor agonists) and LY171555 (a selective dopamine D2 receptor agonist) also induced pial venous constriction exclusively in the presence of L-NNA. The constriction was not affected by phentolamine (10(-6) M). The order of potency for these agonists in the presence of phentolamine, propranolol, guanethidine and L-NNA was: 6-bromo-APB > SKF38393 > dopamine > LY171555. The dopamine-induced constriction in the presence of phentolamine was further inhibited by both SCH23390 (a selective dopamine D1 receptor antagonist) and sulpiride (a selective dopamine D2 receptor antagonist), but was not affected by dopamine D3 or D4 receptor antagonists. These results indicate that dopamine at low and high concentrations induces exclusively constriction of isolated porcine pial veins. The constriction is mediated by postsynaptic alpha2-adrenoceptors, and dopamine D1 and D2 receptors.
authors.affiliation: Department of Pharmacology, Southern Illinois University, School of Medicine, Springfield 62794-1222, USA.
authors.forename: M H
authors.initials: MH
authors.lastname: Sun
authors.forename: T
authors.initials: T
authors.lastname: Ishine
authors.forename: T J
authors.initials: TJ
authors.lastname: Lee
mesh_terms: D058669:Adrenergic alpha-2 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D002550:Cerebral Veins / Q000187:drug effects / Q000502:physiology*; D004298:Dopamine / Q000494:pharmacology / Q000502:physiology*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D017447:Receptors, Dopamine D1 / Q000819:agonists; D017448:Receptors, Dopamine D2 / Q000819:agonists; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D058669:Adrenergic alpha-2 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D004298:Dopamine