Abstract
We sought to determine if redundancy between vasodilators is physiologically relevant during active hyperaemia. As inhibitory interactions between vasodilators are indicative of redundancy, we tested whether vasodilators implicated in mediating active hyperaemia, (potassium (K+), adenosine (ADO) and nitric oxide (NO)), inhibit one anothers vasodilatory effects through direct drug application and during muscle contraction. Using the hamster cremaster muscle and intravital microscopy we locally stimulated capillaries with one vasodilator in the absence and the presence of a second vasodilator (10−7M SNAP, 10−7M ADO, 10 mm KCl) applied sequentially and simultaneously, and observed the response in the associated upstream 4A arteriole controlling the perfusion of the stimulated capillary. We found that KCl significantly attenuated SNAP and ADO-induced vasodilatations by ∼49.7% and ∼128.0% respectively and ADO significantly attenuated KCl and SNAP-induced vasodilatations by ∼94.7% and ∼59.6% respectively. NO significantly attenuated KCl vasodilatation by 93.8% Further, during muscle contraction we found that inhibition of NO production using L-NAME and inhibition of ADO receptors using XAC was effective at inhibiting contraction-induced vasodilatation but only in the presence of K+ release channel inhibition. Thus, only when the inhibiting vasodilator K+ was blocked was the second vasodilator, NO or ADO able to produce effective vasodilatation. Therefore, we show that there are inhibitory interactions between specific vasodilators at the level of the capillary. Further, these inhibitions can be observed during muscle contraction indicating that redundancies between vasodilators are physiologically relevant and influence vasodilatation during active hyperaemia.
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