Influence of neonatal treatment with the pyrethroid insecticide cypermethrin on the development of dopamine receptors in the rat kidney

The influence of neonatal treatment with the pyrethroid insecticide cypermethrin ((R,S)α-cyano-3-phenoxybenzyl(1R,S)-cis-trans-3-(2,2-dichloro-vinyl)-2,2 -carboxylate) on postnatal development of renal dopamine receptors was investigated by radioligand binding assay techniques. Treatment with cypermethrin was made on rats from the 10th to the 16th day after birth. Dopamine D₁- and D₂-like receptors were assayed in frozen sections of kidney of 21-, 30-, 60- and 90-day-old rats using as ligands of dopamine D₁- and D₂-like receptors [³H]([R](+)-(chloro-2,3,4,5,-tetrahydro-5-phenyl-1,4-benzazepinal hemimaleate) (SCH 23390) and [³H]spiperone, respectively. Treatment with cypermethrin was without effect on the affinity (K(d) value) or the density (B(max) value) of dopamine D₁- and D₂-like receptors of rats of 21 days of age. In older groups, treatment with the compound reduced the affinity and increased the density of dopamine D₁-like receptors, whereas it was without effect on the affinity of dopamine D₂-like receptors and decreased their density. These findings indicate that neonatal treatment with the pyrethroid insecticide cypermethrin induces long-lasting impairment of renal dopamine D₁- and D₂-like receptors, and that kidney is a target of the toxic action of the compound. Renal dopamine receptor changes caused by cypermethrin are consistent with possible alterations of renal tubular function and of sympathetic neuroeffector modulation. The above data suggest also that, different from the adult, neonatal exposure to pyrethroid insecticides may induce toxic effects.