Nonesterified fatty acids in the pathogenesis of hypertension: theory and evidence.
This paper approaches the hypothesis that fatty acids contribute to hypertension by examining possible interactions of nonesterified fatty acids with renal pressure-natriuresis, peripheral vascular resistance, and the central nervous barostat, three loci where long-term regulation of blood pressure is probably controlled. By inhibiting aldosterone secretion, nonesterified fatty acids may lower blood pressure by facilitating pressure-natriuresis. Oxygenated metabolites of fatty acids appear to stimulate aldosterone secretion. In different experimental situations, fatty acids either constrict or dilate arteries. There is no evidence of an effect of fatty acids on the central nervous barostat, but they do sensitize peripheral vessels to alpha-adrenergic stimuli. Obesity and diabetes are marked by increased incidence of hypertension, and elevated levels of fatty acids or their P450 oxygenated metabolites may contribute to this association. Drugs that influence plasma fatty acids, like heparin, do not have reproducible effects on blood pressure. Experimental evidence suggests but does not prove that nonesterified fatty acids can affect the long-term set-point of blood pressure.
Goodfriend
T L
TL
William S. Middleton Memorial Veterans Hospital, Madison, WI 53705, USA.
Egan
B M
BM
D000450:Aldosterone / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000494:pharmacology / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D008954:Models, Biological; D009318:Natriuresis / Q000187:drug effects
D005230:Fatty Acids, Nonesterified; D000450:Aldosterone