The involvement of endothelium in the contractile responses of rat aortic rings to phenylephrine and potassium chloride in pregnancy was examined. Contractions in response to both agents were significantly greater in rings from non-pregnant rats than in rings from pregnant rats, and they were unaltered by treatment of the rings with indomethacin. De-endothelialization potentiated the contractions of rings from pregnant rats in response to phenylephrine, but had no significant effect on similar rings contracted with potassium chloride. Whereas de-endothelialization had no significant effect on the contractions to phenylephrine in rings from non-pregnant rats, it decreased those of rings from the same type of rats, contracted with potassium chloride. Pregnancy significantly inhibited contractions in response to calcium chloride of rings treated with phenylephrine or potassium chloride. The effect of endothelium removal on contractions to calcium chloride in rings from pregnant and non-pregnant rats treated with phenylephrine or potassium chloride was similar to that observed for phenylephrine-induced and potassium chloride-induced contractions, respectively. Contractions of intact aortic rings from pregnant and non-pregnant rats to phenylephrine in calcium-free medium were similar. Results of the study suggest that the effect of pregnancy on the contractions of the rat aorta in response to phenylephrine and potassium chloride is at least partly mediated by the endothelium and is independent of prostaglandin synthesis. The endothelial factor involved in this effect appears to modulate contractions by interfering with calcium influx through the receptor-operated calcium channels and the voltage-operated calcium channels.
- Vascular contractility
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