Zero extracellular K+ and prostaglandin E release in the guinea-pig taenia coli

Prostaglandin E release rates from isolated strips of guinea-pig taenia coli increased during exposure to zero K⁺ bathing fluid, from control values of $\text{0.78 ± 0.11}\text{ng/g}$ per min to levels as high as 29.2 ng/per min. Release rates increased for 40–50 min and then remained constant or fell despite progressive increases in intracellular sodium Na_i⁺] or fall in intracellular potassium K_i⁺]. Readmittance of K⁺ to the bathing solution resulted in rapid reversal of elevated prostaglandin E release rates. Na⁺_i] and K⁺_i] were markedly more abnormal in strips exposed to zero K⁺ for 70–201 min compared to 30-min exposures. Upon the readdition of K⁺ after long zero K⁺ exposure, the rate of prostaglandin E release fell long before Na⁺_i] and K⁺_i] returned to control levels. After K⁺ was readded to the bathing solution, the ion concentration of tissues exposed to zero K⁺ for 30 min returned to normal much more quickly than did those of tissues exposed for the longer time periods, yet the exponential rate constants for fall of prostaglandin E release rate after K⁺ was added were not significantly different after short or long zero K⁺ exposure. Thus there was a dissociation between the return of Na⁺_i] and K⁺_i] and the fall of prostaglandin E release rate to control levels. Ouabain augmented prostaglandin E release under conditions where K⁺_i] could not fall. Addition of known neurotransmitters present in this tissue to the bathing fluid did not augment prostaglandin E release. Guinea-pig taenia coli strips that had been incubated with ³H]arachidonic acid, constantly released ³H]arachidonic acid and ³H]prostaglandin E and a prostaglandin which cochromatographed with prostaglandin E but could not be converted to prostaglandin B by alkali and was shown to be 6-ketoprostaglandin F_1α. Release of ³H]arachidonic acid and ³H]prostaglandin E plus 6-³H]ketoprostaglandin F_1α was increased when strips were exposed to zero K⁺. Data obtained in this study suggest the augmented prostaglandin E release seen during zero K⁺ or ouabain is related to increased availability of unbound arachidonic acid at the site of cyclooxygenase in the cell. Augmented prostaglandin E release is apparently not related to alterations in intracellular electrolyte concentrations or release of known neurotransmitters.