Potassium inhibits nitric oxide and adenosine arteriolar vasodilatation via KIR and Na+/K+ATPase: implications for redundancy in active hyperaemia

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Abstract

Redundancy, in active hyperaemia, where one vasodilator can compensate for another if the first is missing, would require that one vasodilator inhibits the effects of another; therefore, if the first vasodilator is inhibited, its inhibitory influence on the second vasodilator is removed and the second vasodilator exerts a greater vasodilatory effect. We aimed to determine whether vasodilators relevant to skeletal muscle contraction [potassium chloride (KCl), adenosine (ADO) and nitric oxide] inhibit one another and, in addition, to investigate the mechanisms for this interaction. We used the hamster cremaster muscle and intravital microscopy to directly visualize 2A arterioles when exposed to a range of concentrations of one vasodilator [10−8 to 10−5 m S-nitroso-N-acetyl penicillamine (SNAP), 10−8 to 10−5 m ADO, 10 and 20 mm KCl] in the absence and then in the presence of a second vasodilator (10−7 m ADO, 10−7 m SNAP, 10 mm KCl). We found that KCl significantly attenuated SNAP-induced vasodilatations by ˜65.8% and vasodilatations induced by 10−8 to 10−6 m ADO by ˜72.8%. Furthermore, we observed that inhibition of KCl vasodilatation, by antagonizing either Na+/K+ ATPase using ouabain or inward rectifying potassium channels using barium chloride, could restore the SNAP-induced vasodilatation by up to ˜53.9% and 30.6%, respectively, and also restore the ADO-induced vasodilatations by up to ˜107% and 76.7%, respectively. Our data show that vasodilators relevant to muscle contraction can interact in a way that alters the effectiveness of other vasodilators. These data suggest that active hyperaemia may be the result of complex interactions between multiple vasodilators via a redundant control paradigm.

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