The role of extracellular calcium in pregnancy-induced attenuation of phenylephrine contraction in rat aorta with functional endothelium.

The effect of pregnancy on the supply of calcium ions for the contractile responses of rat aortic rings to phenylephrine was investigated. The contractility of intact aortic rings from pregnant rats, compared with that of similar rings from non-pregnant rats, to phenylephrine and potassium chloride was significantly decreased. Contractions of rings from non-pregnant rats, pretreated with phenylephrine or potassium chloride, in response to calcium chloride were greater than those of similarly treated rings from pregnant rats. When the concentration of calcium chloride in the medium bathing the rings was reduced to 0.8 mmol.l-1, the contractile response to phenylephrine was significantly (P < 0.005) inhibited in rings from both pregnant and non-pregnant rats but to a greater extent in rings from non-pregnant rats. Contractions of aortic rings from pregnant rats in response to phenylephrine in calcium-free medium were similar to those of rings from non-pregnant rats, suggesting equal dependence on calcium from intracellular stores. The results suggest that pregnancy decreased the response to calcium influx into the aortic smooth muscle cells through both receptor- and voltage-operated calcium entry pathways. Since de-endothelialization reversed the pregnancy-induced diminished contraction to phenylephrine, it is likely that pregnancy interfered with contractions induced by activation of receptors with phenylephrine through enhanced production of endothelium-derived relaxing factor(s).