Evidence for enhanced venous smooth muscle turnover of prostaglandin-like substance in portal veins from spontaneously hypertensive rats.

The sensitivity of portal veins from 14 to 18 week-old Okamoto-Aoki spontaneously hypertensive rats to prostaglandins A2, B2, D2 and F2alpha were enhanced whereas the sensitivity to prostaglandin E2 was diminished when compared with responses of veins from normotensive Wistar-Kyoto rats. Inhibition of prostaglandin synthesis with both eicosotetraynoic acid (ETYA) and indomethacin (INDO) abolished the observed differences in sensitivity to prostaglandins. Synthesis of prostaglandin-like substance (with arachidonic acid as precursor) was significantly enhanced in portal veins from spontaneously hypertensive rats. Metabolism of prostaglandins E2 and F2alpha, employing the oil-immersion technique of Kalsner and Nickerson, appeared to be similar in veins from normotensive and hypertensive rats. These findings suggest that prostaglandin synthesis is enhanced in venous smooth muscle from hypertensive rats. The increased concentration of endogenous prostaglandin at the venous smooth muscle cell may modify the responses to exogenously administered prostaglandins thus accounting, in part, for the altered sensitivity to these fatty acids.