Prostaglandins.

A discussion of important aspects of the effects of prostaglandins on arteries must include (a) the nature of the receptors for the different humoral agents, (b) the potential modulatory role that endogenously produced prostaglandins may play when other vasoactive hormones are present, and (c) the potential for cell-to-cell transfer of substrates for formation of novel biologically active arachidonic acid metabolites. Evidence suggests that at least two vasodilator receptors for prostaglandins exist (PGE2 and PGI2) and at least one vasoconstrictor receptor (TXA2), probably more. Activation of vasodilator mechanisms by endogenously produced vasodilator prostaglandins in isolated arteries or in vivo can attenuate the vasoconstrictor activity of angiotensin II and in some cases mediate the vasodilator effects of bradykinin. Perhaps the most important source of vasoactive arachidonic acid metabolites may be the interaction of blood cells with the vessel wall. Platelets produce thromboxane (TXA2), which has vasoconstrictor effects at 10(-8) M in vitro. Diversion of the precursor from the platelet by selective inhibition of thromboxane synthetase can provide substrate for vascular PGI2 synthesis. Other interactions between leukocytes, platelets, endothelium cells, and smooth-muscle cells are likely to reveal further pathways for the formation of vasoactive arachidonic acid metabolites.