Neuroeffector actions of prostaglandins on isolated arteries.

PGD2, PGF2 alpha, and CTA2 are compounds that increase vascular contractility indirectly by potentiating responses to nerve stimulation or vasoconstrictor agents and directly by acting on vascular smooth-muscle receptors. The direct vasoconstrictor potency is in the order of CTA2 greater than PGF2 alpha greater than PGD2 (5,6,9). The ratio of concentrations for directly- and indirectly-induced contractions is approximately 1,000 with PDG2, 100 with PGF2 alpha, and 10 with CTA2. PGD2, PGF2 alpha, and TXA2 may contribute to provoking coronary vasospasm because of potentiating actions on responses to adrenergic and other vasoconstrictor stimuli and to their vasoconstrictor actions. The former effect is induced by appreciably lower concentrations. On the other hand, PGI2 appears to counteract responses to the vasoconstrictor interventions. PGD2 and PGF2 alpha act on presynaptic receptors and increase the release of norepinephrine; these actions are resistant to diphloretin, a PG antagonist. In contrast, CTA2 and PGI2 act on postsynaptic receptors and alter smooth-muscle reactivity to vasoconstrictors; these actions are sensitive to the PG antagonist.