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arachidonic acid. The exact mechanism of PGA formation has not been studied intensively, but it is believed to be the result of chemical dehydration at C-10,11 with introduction of a double bond at this site. There is little free unsaturated fatty acid inside cells, and it is believed that these precursors are stored as membranes phospholipids or as membrane sterol esters or both. There is evidence that the major rate-limiting enzymes in prostaglandin synthesis are not only PG synthesize but also cholesterol esterase and phospholipase A, which catalyze the hydrolysis of the unsaturated fatty acids from cholesterol and phospholipids respectively.
BIOLOGIC ACTIONS The biologic actions of the prostaglandins are the most varied of any naturally occurring compound. The nonvascular actions of the prostaglandins are closely linked to changes in 3’,5’-cyclic AMP (C-AMP). In this regard, it is important to note that unlike other hormones affecting C-AMP, the same prostaglandin can in some tissues increase and in others decreases adenyl cyclase and C-AMP. A role for prostaglandin interaction with CAMP in the cardiovascular system has yet to be established
CARDIOVASCULAR-RENAL SYSTEM Antihypertensive Renal Function
A growing body of evidence suggests that the kidney, in addition to secreting the well-known renal pressor hormones, such as those of the renal rennin-angiotensin system, also has an antihypertensive endocrine function. It is thought that the state of hypertension may be the result of a deficiency of renal vasodepressor substances which allow pressor mechanisms to act unopposed in bringing about peripheral arteriolar constriction and an ensuing rise in blood pressure. The isolation from the rabbit renal medulla of the vasodilating prostaglandin, medullin (subsequently renamed PGA,), provided the first demonstration that the kidney possessed a specific antihypertensive compound (3,4). The vasodepressor prostaglandin PGE, was also located and identified in rabbit renal medulla. However, its effects on nonvascular smooth muscle, its rapid metabolism by the lung, and its different metabolic and hypotensive mechanisms seem to exclude PGE, as a circulating antihypertensive hormone.
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