Potassium augments vascular relaxation mediated by nitric oxide in the carotid arteries of hypertensive Dahl rats.
The present study was designed to determine whether and how potassium supplementation improves the endothelial function of carotid arteries of hypertensive Dahl rats. Dahl salt-sensitive rats were fed a high sodium diet, a high sodium plus potassium-supplemented diet, a normal rat chow, or a potassium-supplemented diet for 4 weeks. High sodium intake significantly increased the blood pressure, which was attenuated by potassium supplementation. The isometric tension of rat-isolated carotid rings was measured. In norepinephrine-precontracted rings, the relaxation in response to acetylcholine, adenosine 5'-diphosphate (ADP), and isoproterenol were significantly attenuated in hypertensive Dahl rats, which was improved by potassium supplementation. Pretreatment with N(G)-nitro-L-arginine methyl ester blocked the responses to acetylcholine and ADP, and eliminated the difference in relaxation in response to isoproterenol. The endothelium-independent relaxation in response to forskolin, S-nitroso-N-acetyl-DL-penicillamine, and sodium nitroprusside was significantly attenuated in hypertensive Dahl rats, which was not affected by potassium supplementation. The results indicated that salt-induced hypertension was associated with marked alterations in the endothelial and vascular smooth muscle functions of the carotid arteries of Dahl rats. Potassium supplementation ameliorated the endothelial but not the smooth muscle function. The protective effect of potassium appeared to be achieved through increased endothelial nitric oxide production. The current studies, in conjunction with our recent studies on nitric oxide synthase activity in the kidney, strongly suggest that potassium attenuates development of hypertension by increasing nitric oxide production in Dahl rats.
2nd Department of Physiology, Kagawa Medical University, Kida, Japan.
M S
MS
Zhou
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H
Kosaka
H
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Yoneyama
D000109:Acetylcholine / Q000494:pharmacology; D000244:Adenosine Diphosphate / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002339:Carotid Arteries / Q000187:drug effects / Q000503:physiopathology*; D005576:Colforsin / Q000494:pharmacology; D019587:Dietary Supplements; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006973:Hypertension / Q000097:blood / Q000503:physiopathology* / Q000652:urine; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009566:Nitrates / Q000652:urine; D009569:Nitric Oxide / Q000494:pharmacology*; D009573:Nitrites / Q000652:urine; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D010396:Penicillamine / Q000031:analogs & derivatives* / Q000494:pharmacology; D017419:Potassium, Dietary / Q000494:pharmacology*; D051381:Rats; D020303:Rats, Inbred Dahl; D026423:S-Nitroso-N-Acetylpenicillamine; D012965:Sodium Chloride / Q000633:toxicity; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology*
D000318:Adrenergic beta-Agonists; D004791:Enzyme Inhibitors; D009566:Nitrates; D009573:Nitrites; D017419:Potassium, Dietary; D014665:Vasodilator Agents; D009599:Nitroprusside; D005576:Colforsin; D019335:Nitroarginine; D009569:Nitric Oxide; D012965:Sodium Chloride; D000244:Adenosine Diphosphate; D026423:S-Nitroso-N-Acetylpenicillamine; D000254:Sodium-Potassium-Exchanging ATPase; D010396:Penicillamine; D007545:Isoproterenol; D000109:Acetylcholine