Rhythmic contractions in isolated small arteries of rat: role of K+channels and the Na+, K+‐pump

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Abstract
Small mesenteric arteries from Wistar rats display rhythmic tension oscillations, associated with oscillations in membrane potential, when stimulated with noradrenaline. The purpose of this study was to investigate the role of potassium conductance and Na+, K+‐pump activity in the generation of these oscillations. The effect on the rhythmic contractions of several agents, interacting with K+channels, was studied. Application of apamin, pinacidil or glibenclamide did not affect the rhythmic activity. Tetraethylam‐monium (TEA) increased the frequency of the rhythmic contractions, while application of 4‐aminopyridine (4‐AP) increased the amplitude by approximately 50%, with no changes in frequency. Ba2+, on the other hand, impaired the rhythmic contractions or converted them to irregular oscillations in the presence of functional endothelium, but did not affect oscillations in endothelium‐denuded vessels. Ouabain or exposure to K+‐free solution, procedures known to inhibit the Na+, K+‐pump, abolished the rhythmic contractions. This effect was immediate, suggesting that it was due to elimination of the electrogenic action of the Na+, K+‐ATPase, rather than to a change in intracellular ion concentrations. Exposure to an extracellular potassium concentration of more than 20 mM also inhibited the oscillation activity. The results suggest that the oscillations are not caused by, but may be modulated by, variations in potassium conductance. The Na+, K+‐pump seems to play an important role in the generation of rhythmic contractions in these vessels.