Effect of prostacyclin and 9a, 11a-epoxymethanoprostaglandin H2 on calcium and magnesium fluxes and tension development in canine intralobar pulmonary arteries and veins.

Calcium and magnesium ions modulate the responses of canine vascular smooth muscle to prostaglandins (PGs). This study was designed to evaluate the relationship between the effects of prostacyclin (PGI2) and 9a, 11a-epoxymethanoPGH2 (EMP) on calcium and magnesium fluxes and tension development of the canine intralobar pulmonary arteries (IPA) and veins (IPV). PGI2 produced relaxation of canine IPA and IPV, decreased the uptake of 45Ca and increased the accumulation of 28Mg into an intracellular or tightly bound pool of divalent ion. The efflux of both calcium and Magnesium were not affected by PGI2. 6-Keto-PGF1a, the inactive metabolite of PGI2, did not affect the efflux or uptake of either Calcium or Magnesium, and did not produce any change in the basal tone of IPA or IPV. IPA and IPV contracted when challenged with EMP. The contractile responses of the IPA and IPV to EMP were associated with an increase in the efflux of Calcium from a tightly bound pool of calcium ion and a decrease in the uptake of 28Mg into these blood vessels. These data support the conclusions that: 1) PGI2-induced relaxation of IPA and IPV may be mediated by a decrease in the influx of activator calcium ion and an increase in the influx of modulator magnesium ion; 2) EMP-induced contraction of IPA and IPV appears to result from a release of calcium ion from a tightly bound site within the vascular smooth muscle cell; and 3) the effects of PGI2 and EMP on magnesium ion may result from a direct action of these prostanoids on the mechanisms regulating magnesium fluxes or they may be secondary to the alterations in the fluxes of calcium ion.