Moderate Elevation of Extracellular K<SUP>&#8290;</SUP> Concentration Induces Vasorelaxation in Isolated Rat, Rabbit and Human Cerebral Arteries Role of Na Pump and Ba-Sensitive Process

Moderate Elevation of Extracellular K<SUP>&#8290;</SUP> Concentration Induces Vasorelaxation in Isolated Rat, Rabbit and Human Cerebral Arteries Role of Na Pump and Ba-Sensitive Process

<P> Cerebral blood vessels relax when extracellular K<SUP>&#8290; </SUP>concentrations ([K<SUP>&#8290;</SUP>])<SUB>e</SUB> are elevated moderately (2∼15 mM, K<SUP>&#8290;</SUP>-induced vasorelaxation). We have therefore studied the underlying mechanism for this K<SUP>&#8290;</SUP>- induced vasorelaxation in the isolated middle cerebral arteries (MCAs). The effects of ouabain and Ba<SUP>2&#8290; </SUP>on K<SUP>&#8290;</SUP>-induced vasorelaxation were examined to determine the role of sodium pump and/or Ba-sensitive process (possibly, inward rectifier K current) in the mechanism. Mulvany myograph was used to study 24 rats, 18 rabbits, and 10 humans MCAs (216&#8273;3 &#12557;m, 347&#8273;7 &#12557;m, and 597&#8273;39 &#12557;m in diameter when stretched to a tension equivalent to 55 mmHg). High K<SUP>&#8290;</SUP> (125 mM) and PGF<SUB>2α</SUB> (1∼10 &#12557;M) induced concentration-dependent contractions in all 3 species, while histamine (10∼50 &#12557;M) evoked contraction only in the rabbits and induced relaxation in the rats and humans. Addition of K<SUP>&#8290; </SUP>(2∼10 mM) to the control solution induced vasorelaxations. These effects were inhibited by the pretreatment with both ouabain (10 &#12557;M) and Ba<SUP>2&#8290;</SUP> (0.1∼0.3 mM) in the rat, but only with ouabain (10 &#12557;M) in the rabbit and human. These results suggest that K<SUP>&#8290;</SUP>-induced vasorelaxation occurs via the stimulation of electrogenic Na pump in the rabbit and human MCAs, while in the rat MCAs via the activation of both Na pump and Ba-sensitive process.