Prejunctional and postjunctional actions of prostaglandins F2 alpha and I2 and carbocyclic thromboxane A2 in isolated dog mesenteric arteries.

Prostaglandin (PG) F2 alpha in concentrations insufficient to alter the basal tone potentiated contractile responses of helical strips of dog mesenteric arteries to transmural electrical stimulation but did not alter the responses to norepinephrine. Carbocyclic thromboxane A2 (cTxA2) potentiated the response to transmural stimulation, norepinephrine, serotonin and angiotensin II. PGI2 (up to 10(-7) M) attenuated the contraction induced by transmural stimulation, norepinephrine and serotonin. The potentiating effect of PGF2 alpha was not antagonized by diphloretin phosphate, a PG antagonist, whereas the effects of cTxA2 and PGI2 were prevented. 3H Overflow evoked by transmural stimulation in superfused arterial strips previously soaked in media containing [3H]norepinephrine was increased by PGF2 alpha but was not altered by cTxA2 and PGI2. It may be concluded that PGF2 alpha potentiates the contractile response to adrenergic nerve stimulation by increasing the release of norepinephrine, and that cTxA2 potentiates the response by increasing arterial muscle contractility, whereas PGI2 attenuates contractility. Prejunctional effects of PGs appear to be mediated by receptive sites different from those located postjunctionally.