Abstract
The prostaglandins are generated de novo at the time of a physiologic stimulus. Once formed they are rapidly inactivated by a variety of enzymatic mechanisms. They exhibit a variety of physiologic actions involving changes in muscle contractility, secretion, lipolysis, differentiation, replication, aggregation, and permeability. Many of these effects appear to be mediated through changes in CAMP or cGMP.‘* ’ At the time prostaglandins were first described, interest was centered on their possible role as circulating hormones. Their effects on tissue CAMP concentrations suggested a possible analogy with polypeptide hormones which generally act by this mechanism. Since the usual effect of the E prostaglandins was to dilate blood vessels, their possible involvement in the control of systemic blood pressure received particular attention. In subsequent studies, however, the rapidity with which E and F prostaglandins are inactivated in the circulation became appreciated and the concept of a local modulatory action began to emerge. While an important role in regulating systemic blood pressure
Published Version
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