Potassium effects on contraction in arterial smooth muscle mediated by Na+, K+-ATPase.
A local increase in the extracellular potassium concentration [K+]o, up to about 8 meq/liter either by topical application or intra-arterial infusion of K+ salts, causes arteriolar dilation and decreased resistance to blood flow in systemic vascular beds. Isolated vascular smooth muscle responds to a similar increase in [K+] in the bathing fluid with relaxation if the preparation has some initial active tension. Reduction in [K+] over physiological ranges produces arteriolar constriction and increased resistance to blood flow. K+ vasodilation is accompanied by hyperpolarization of the smooth muscle cell whereas the vasoconstriction is accompanied by depolarization. All these responses can be blocked by ouabain, a potent Na+, K+-ATPase inhibitor. It is therefore thought that K+ vasodilation results from stimulation of the electrogenic Na+-K+ pump whereas the vasoconstriction results from inhibition of this pump. A number of conditions that alter resistance also alter interstitial fluid [K+]. These include exercise, myocardial ischemia, epileptic convulsions, and evoked electrical activity of the somatomotor cortex. Certain findings, including those during administration of ouabain, suggest that changes in [K+] contribute significantly to some of the changes in resistance.
D000818:Animals; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000201:enzymology; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology*; D012413:Rubidium / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D012413:Rubidium; D011188:Potassium