Acute lead exposure and contraction of rat isolated aorta induced by D1-dopaminergic and alpha-adrenergic drugs.

BACKGROUND/OBJECTIVE In the present study, the effect of acute lead exposure in the presence and absence of dopamine or alpha (alpha)-adrenoceptor agents on contractile response of rat isolated thoracic aorta was studied. METHODS Male Wistar rats were used in all experiments. Thoracic aorta was carefully removed, cleaned, and cut into 2-mm thick rings. The rings were mounted for measurement of isometric contractions in a tissue bath containing 10 mL of Kreb's solution at 37 - 38 degrees C. The following drugs were used: lead chloride, dopamine, phenylephrine, prazosin, clonidine, yohimbine, and SCH23390. One-way analysis of variance (ANOVA) and Student's t-test were used for statistical analyses. P < 0.05 was considered significant. RESULTS The alpha1-adrenoceptor antagonist (prazosin), alpha2-adrenoceptor antagonist (yohimbine), or dopamine D1 receptor antagonist (SCH23390), did not elicit any response. Combination of lead with dopamine, phenylephrine, or clonidine did not show any potentiation. SCH23390, prazosin, and yohimbine decreased the contraction induced by lead. SCH23390 decreased the contraction induced by dopamine, or lead plus dopamine. Prazosin reduced the contraction induced by phenylephrine or lead plus phenylephrine. Yohimbine attenuated the response induced by clonidine or lead plus clonidine. CONCLUSION alpha1, alpha2, and D1 dopamine receptor mechanisms could have a role in lead-induced contraction.