The role of prostaglandins in human hypertension.
A large body of evidence supports the concept that prostaglandins (PG) are importantly involved in arterial pressure regulation. Various PGs, especially PGE2 and prostacyclin (PGI2) may influence blood pressure through control of vascular tone, sodium excretion, and renin release. Inhibition of PG synthesis by nonsteroidal antiinflammatory drugs (NSAID) augments the vasoconstrictor response to exogenous pressors such as angiotensin II, arginine vasopressin (AVP), and fludrocortisone. The acute administration of NSAID to either normotensive or untreated hypertensive subjects results in an increase in arterial pressure and peripheral resistance; long-term administration, however, is associated with little or no change in blood pressure, possibly because of a reduction in cardiac output. Although NSAID have little influence on blood pressure in normotensive subjects or untreated hypertensives, inhibition of PG synthesis blunts or abolishes the antihypertensive effect of most antihypertensive agents. NSAID antagonize the vasodepressor action of diuretics, beta-adrenoreceptor antagonists, vasodilators, and converting enzyme inhibitors. Consequently, potent NSAID should be used with caution, if at all, during treatment of hypertensive patients. Numerous studies have examined renal PG production in essential hypertension (EH). The majority have demonstrated reduced basal and stimulated urinary PGE2 excretion in EH compared to normotensive subjects, but there is substantial overlap. Nevertheless, renal PGE2 synthesis is significantly decreased in approximately one-third of patients with EH. A recent innovative approach to arterial pressure regulation has focused on dietary supplementation with polyunsaturated fatty acids (PUFA), especially linoleic acid and eicosapentaenoic acid. Several groups have demonstrated that long-term dietary supplementation with PUFA reduces blood pressure in both normotensive individuals and in patients with EH.(ABSTRACT TRUNCATED AT 250 WORDS)
D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D016861:Cyclooxygenase Inhibitors; D004041:Dietary Fats / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D011453:Prostaglandins / Q000096:biosynthesis / Q000494:pharmacology / Q000502:physiology*; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects
D000893:Anti-Inflammatory Agents; D016861:Cyclooxygenase Inhibitors; D004041:Dietary Fats; D005231:Fatty Acids, Unsaturated; D011453:Prostaglandins