Regulatory Mechanism of Vascular Contractility by Extracellular K+ : Effect on Endothelium-Dependent Relaxation and Vascular Smooth Muscle Contractility.
- Author:
Ji Young YOU
1
;
Geun Hee SEOL
;
Suk Hyo SUH
;
Jae Ho AHN
Author Information
1. Department of Emergency Medicine, Kangdong Sacred Heart Hospital, Hallym University, Korea.
- Publication Type:Original Article
- Keywords:
Potassium;
Vasodilation;
Endothelium-dependent relaxing factor;
Calcium
- MeSH:
Acetylcholine;
Adenosine Triphosphate;
Animals;
Aorta;
Arteries;
Basilar Artery;
Calcium;
Carotid Arteries;
Dinoprost;
Endothelial Cells;
Endothelium;
Endothelium-Dependent Relaxing Factors;
Humans;
Isometric Contraction;
Mesenteric Artery, Superior;
Mesentery;
Mice;
Muscle, Smooth, Vascular*;
Nitric Oxide;
Nitroarginine;
Norepinephrine;
Ouabain;
Potassium;
Relaxation*;
Umbilical Veins;
Vasodilation
- From:The Korean Journal of Thoracic and Cardiovascular Surgery
2004;37(3):210-219
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Extracellular K+ concentration ([K+]o) can be increased within several mM by the efflux of intracellular K+. To investigate the effect of an increase in [K+]o on vascular contractility, we attempted to examine whether extracellular K+ might modulate vascular contractility, endothelium-dependent relaxation (EDR) and intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells (EC). MATERIAL AND METHOD: We observed isometric contractions in rabbit carotid, superior mesentery, basilar arteries and mouse aorta. [Ca2+]i was recorded by microfluorimeter using Fura-2/AM in EC. RESULT: No change in contractility was recorded by the increase in [K+]o from 6 to 12 mM in conduit artery such as rabbit carotid artery. whereas resistant vessels, such as basilar and branches of superior mesenteric arteries (SMA), were relaxed by the increase. In basilar artery, the relaxation by the increase in [K+]o from 1 to 3 mM was bigger than that by the increase from 6 to 12 mM. In contrast, in branches of SMA, the relaxation by the increase in [K+]o from 6 to 12 mM is bigger than that by the increase from 1 to 3 mM. Ba2 (30microM) did not inhibit the relaxation by the increase in [K+]o from 1 to 3 mM but did inhibit the relaxation by the increase from 6 to 12 mM. In the mouse aorta without the endothelium or treated with NG-nitro-L-arginine (30microM), nitric oxide synthesis blocker, the increase in [K+]o from 6 to 12 mM did not change the magnitude of contraction induced either norepinephrine or prostaglandin F2alpha. The increase in [K+]o up to 12 mM did not induce contraction of mouse aorta but the increase more than 12 mM induced contraction. In the mouse aorta, EDR was completely inhibited on increasing [K+]o from 6 to 12 mM. In cultured mouse aorta EC, [Ca2+]i was increased by acetylcholine or ATP application and the increased [Ca2+]i was reduced by the increase in [K+]o reversibly and concentration-dependently. In human umbilical vein EC, similar effect of extracellular K+ was observed. Ouabain, a Na+-K+ pump blocker, and Ni2 , a Na+-Ca2+ exchanger blocker, reversed the inhibitory effect of extracellular K+. CONCLUSION: In resistant arteries, the increase in [K+]o relaxes vascular smooth muscle and the underlying mechanisms differ according to the kinds of the arteries; Ba2 -insensitive mechanism in basilar artery and Ba2 -sensitive one in branches of SMA. It also inhibits [Ca2+]i increase in EC and thereby EDR. The initial mechanism of the inhibition may be due to the activation of Na+-K+ pump.
