Myocardial Infarction

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PGs play important roles in a number of organ systems, including the central nervous system, blood platelets (as described in this chapter), smooth muscles of the respiratory tract (also described here in connection with asthma), peripheral nervous system, gastrointestinal tract, and cardiovascular system. In the kidney, PGs, possibly mainly PGAs, produce vasodilation and accelerate the removal of sodium ion into the urine. PGs apparently can act in the opposite direction by stimulating the renin-angiotensin-aldosterone system. In this case, as in many others, opposing actions of PGs occur as a homeostatic mechanism. Nonsteroidal anti-inflammatory drugs, if administered chronically, can compromise the hypotensive activity of PGs in the kidney.

There is some reason to believe that activated platelet activity may play a role in plaque formation if the reaction is overresponsive and can also contribute to some instances of myocardial infarction. Thus, TX production by platelets would be balanced by PGI2 production. "Sticky" platelets could have a negative effect on the development of myocardial infarction over the long term, and some claims have been made that chronic aspirin users could have a lower incidence of myocardial infarction, the explanation being that TX

Cell membrane phospholipid Phospholipase A, w y

Arachidonate Lyso-glyceryl-

phosphorylcholine t

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