Arachidonic acid metabolites, hypertension and arteriosclerosis.
The level of arterial blood pressure is set by complete interactions of several mechanisms which influence both blood flow in and resistance of the vascular system. An imbalance favouring elevation of vascular resistance or extracellular volume will result in hypertension. Such alterations may include increased activity of the sympathetic nervous system, of the renin-angiotensin system, or excessive secretion of mineralocorticoids. Of equal importance may be a reduced activity of blood pressure-lowering factors such as prostaglandins and the kallikrein-kinin system. This paper describes the possible significance of prostaglandins in the pathophysiology of hypertension and in degenerative vascular disease, based on their involvement in the control of vascular resistance, renal regulation of extracellular volume and platelet-vessel wall interactions. An abnormality in the biosyn-thesis of certain prostaglandin endoperoxide metabolites may lead to hypertension even without an increase in the activity of the classic blood-pressure-elevating systems. The contribution of prostaglandins for the development of hypertension and degenerative vascular disease may be based on an inherent abnormality of the prostaglandin system, as well as on the effects of major risk factors such as dietary intake of sodium and fat on prostaglandin synthesis. Specific blockade or stimulation of distinct biosynthetic pathways leading to antagonistically acting prostaglandins and nutritional manipulation of precursor fatty acids should lead to a better understanding of the pathomechanisms involved and may offer new strategies for therapy or prevention of these cardiovascular disorders.
D001095:Arachidonic Acids / Q000378:metabolism / Q000502:physiology*; D001161:Arteriosclerosis / Q000503:physiopathology*; D001241:Aspirin / Q000494:pharmacology; D015232:Dinoprostone; D006801:Humans; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D010973:Platelet Adhesiveness / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis / Q000502:physiology*; D011458:Prostaglandins E / Q000378:metabolism; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors
D001095:Arachidonic Acids; D011453:Prostaglandins; D011458:Prostaglandins E; D013928:Thromboxane A2; D015232:Dinoprostone; D001241:Aspirin