Protective effect of dietary potassium against vascular injury in salt-sensitive hypertension.
Hypertensive cardiovascular damage is accelerated by salt loading but counteracted by dietary potassium supplementation. We suggested recently that antioxidant actions of potassium contribute to protection against salt-induced cardiac dysfunction. Therefore, we examined whether potassium supplementation ameliorated cuff-induced vascular injury in salt-sensitive hypertension via suppression of oxidative stress. Four-week-old Dahl salt-sensitive rats were fed a normal-salt (0.3% NaCl), high-salt (8% NaCl), or high-salt plus high-potassium (8% KCl) diet for 5 weeks, and some of the rats fed a high-salt diet were also given antioxidants. One week after the start of the treatments, a silicone cuff was implanted around the femoral artery. Examination revealed increased cuff-induced neointimal proliferation with adventitial macrophage infiltration in arteries from salt-loaded Dahl salt-sensitive rats compared with that in arteries from non-salt-loaded animals (intima/media ratio: 0.471+/-0.070 versus 0.302+/-0.037; P<0.05), associated with regional superoxide overproduction and reduced nicotinamide-adenine dinucleotide phosphate oxidase activation and mRNA overexpression. On the other hand, simultaneous potassium supplementation attenuated salt-induced neointimal hyperplasia (intima/media ratio: 0.205+/-0.012; P<0.001), adventitial macrophage infiltration, superoxide overproduction, and reduced nicotinamide-adenine dinucleotide phosphate oxidase activation and overexpression. Antioxidants, which decrease vascular oxidative stress, also reduced neointima formation induced by salt excess. In conclusion, high-potassium diets seems to have a protective effect against the development of vascular damage induced by salt loading mediated, at least in part, through suppression of the production of reactive oxygen species probably generated by reduced nicotinamide-adenine dinucleotide phosphate oxidase.
D000098:Acetophenones / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D003250:Constriction; D003497:Cyclic N-Oxides / Q000494:pharmacology; D005263:Femoral Artery / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D006973:Hypertension / Q000139:chemically induced* / Q000473:pathology*; D007527:Isoenzymes / Q000235:genetics; D008264:Macrophages / Q000473:pathology; D008297:Male; D019255:NADPH Oxidases / Q000235:genetics; D018384:Oxidative Stress / Q000187:drug effects; D017419:Potassium, Dietary / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D020303:Rats, Inbred Dahl; D017382:Reactive Oxygen Species / Q000378:metabolism; D017673:Sodium Chloride, Dietary / Q000494:pharmacology; D013113:Spin Labels; D017539:Tunica Intima / Q000187:drug effects / Q000473:pathology
D000098:Acetophenones; D000975:Antioxidants; D003497:Cyclic N-Oxides; D007527:Isoenzymes; D017419:Potassium, Dietary; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D017673:Sodium Chloride, Dietary; D013113:Spin Labels; C056165:acetovanillone; D019255:NADPH Oxidases; C001803:tempol