ABSTRACT
As with all humoral agents, two conditions must be satisfied in order for a cell to respond to a prostaglandin. First, the cell must possess the appropriate receptor-response machinery, and second, the concentration of prostaglandin must be high enough to permit occupancy of a sufficient number of receptors to evoke a response. Due to a combination of dilution and catabolism, the concentrations of prostaglandin derivatives in the circulation are too low, except in a few instances, 1,2 to elicit most biological responses. 3,10 Thus, physiologically important responses to prostaglandins are likely to occur only at or near sites of biosynthesis where prostaglandin concentrations can become elevated. As a rule, cells that synthesize a particular prostaglandin will respond to that prostaglandin. 11,17 However, there are cells that respond to but do not synthesize a particular prostaglandin; for example, platelets do not form PGI2, but PGI2 inhibits platelet aggregation 15,16 and the medullary thick ascending limb of Henle’s loop does not synthesize PGE2, 18 but PGE2 inhibits chloride ion resorption in this segment of the nephron. 19 These observations lead to the working hypothesis that prostaglandins synthesized by one cell affect both the parent cell and certain receptive neighboring cells. In this way, prostaglandins serve as intercellular messengers that function to coordinate biological responses requiring the participation of more than one cell type. 20 Three examples of prostaglandins apparently functioning in this manner are in the regulation of hemostasis by TXA2 synthesized by platelets 15,17 and by PGI2 synthesized by the vascular endothelium 15,17 and in the regulation of tubular NaCl resorption in the kidney by PGE 2formed by collecting tubules. 11-14,18-20
