Abstract
Based upon the ability of the E-prostaglandins to stimulate cyclic AMP formation in a dose-related manner and the correlation between this property and their affinity for a membraneous receptor, the action of these prostaglandins was proposed to be expressed largely via cyclic AMP. The failure of the F-prostaglandins to demonstrate significant activity in these two parameters led to the suggestion that they must act at another receptor via a different mediator. The recent isolation of a receptor unique to PGF 2α and the demonstrated ability of this prostaglandin to increase tissue cyclic GMP levels are consistent with this concept that the E-prostaglandins and PGF 2α play distinctly different roles in cell regulation.
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