Korean J Thorac Cardiovasc Surg.  2004 Mar;37(3):210-219.

Regulatory Mechanism of Vascular Contractility by Extracellular K+ : Effect on Endothelium-Dependent Relaxation and Vascular Smooth Muscle Contractility

• You JY
• Seol GH
• Suh SH
• Ahn JH

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.

Keyword

Potassium; Vasodilation; Endothelium-dependent relaxing factor; Calcium

MeSH Terms

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
Acetylcholine
Adenosine Triphosphate
Calcium
Dinoprost
Endothelium-Dependent Relaxing Factors
Nitric Oxide
Nitroarginine
Norepinephrine
Ouabain
Potassium