ABSTRACT
The effect of increased extracellular potassium ([K]o) on rat isolated mesenteric arteries, constricted with phenylephrine, was studied. An increase of [K]o from 5.9mM to 11.2 or 21.2mM caused contraction of arteries with or without endothelium. Decreasing [K]o from 5.9mM to 1.2mM for 3min followed by increase in [K]o to between 5.9mM and a maximum of 41.2mM, induced relaxation. Raising [K]o from a range of concentrations, between 1.2 and 5.9mM, to 13.8mM resulted in a relaxation whose amplitude and duration was inversely proportional to the initial [K]o. The relaxation induced by an increase of [K
]o from 1.2 to 13.8mM was abolished by ouabain or by substituting extracellular sodium by choline or TRIZMA hydrochloride. The relaxations evoked by an increase of [K]o from a low initial concentration may reflect a build-up of intracellular sodium and the subsequent upturn of electrogenic Na,K-ATPase pumping when extracellular potassium is increased. Thus, potassium-induced relaxation involves an ouabain-sensitive mechanism that is dependent on external sodium, but independent of the endothelium.
