Prostaglandins and hypertension.
Generalized arteriolar vasoconstriction is the dominant element in essential hypertension. Although the proximate cause of this process remains elusive, several lines of evidence suggest that abnormalities in prostaglandin and thromboxane metabolism may contribute to the pathophysiology of hypertension. Diminished endogenous synthesis of vasodilator prostaglandins and enhanced formation of the vasoconstrictor thromboxane may participate in this process, particularly in the kidney. The use of nonsteroidal anti-inflammatory drugs, which inhibit prostaglandin synthesis, may aggravate blood pressure control, especially when used with certain diuretics and other antihypertensive medications. Attempts to enhance endogenous synthesis of prostaglandin metabolites expressing potent vasodilator properties by supplementation of the diet with polyunsaturated fatty acids may provide a new strategy to control blood pressure.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001794:Blood Pressure; D002216:Captopril / Q000037:antagonists & inhibitors / Q000494:pharmacology; D004041:Dietary Fats / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D011453:Prostaglandins / Q000378:metabolism / Q000502:physiology*; D012079:Renal Circulation; D013931:Thromboxanes / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D004041:Dietary Fats; D005231:Fatty Acids, Unsaturated; D011453:Prostaglandins; D013931:Thromboxanes; D002216:Captopril