Vasodilators produced during active hyperaemia interact: potassium attenuates the vasodilatory effect of nitric oxide

Abstract

We previously demonstrated that multiple vasodilators (i.e. nitric oxide (NO), potassium (K+), adenosine (ADO)) are produced in response to skeletal muscle contraction and their ability to produce significant vasodilation differ depending on skeletal muscle stimulation parameters. Given the production of multiple vasodilators resulting from muscle contraction we sought to determine whether the dilators produced altered one another's vasodilatory ability. We tested whether NO's vasodilatory effect was altered in the presence of K+. Using the hamster cremaster muscle preparation in situ we used intravital microscopy to observe arteriolar vasodilation in response to a range of concentrations of an NO donor, S‐nitroso‐N‐acetyl pennicillamine (SNAP, 10−8M‐10−4M) in the absence and the presence of 10mM K+. The vasodilation with 10−8M‐10−4M SNAP (3.1±1.0μm, 7.6±1.4μm, 10.0±1.7μm, 15.7±2.3μm, 17.8±2.1μm respectively) was significantly attenuated in the presence of 10mM K+ (−1.9±1.1μm, −0.2±1.5μm, 1.3±2.5μm, 6.5±3.1μm, 11.5±2.8μm respectively). Our data show that K+ significantly attenuates the vasodilatory effect of NO. Thus, active hyperaemia may not be the sum effects of multiple individual vasodilators but a product of their interactions. This research was funded by NSERC, Canada.