Endothelial Contributions to Myogenic and Reactive Dilation
Authors:Joseph Chin, Samara Jasperse
Mentor:Jeffrey Jasperse, Professor of Sports Medicine, Pepperdine University
Arteries briefly dilate in response to an increase in pressure (myogenic dilation). It is not known whether this response is passive or active. Previously, this lab found that arteries actively dilate in response to a brief reduction in intraluminal pressure (reactive dilation), where the magnitude of the dilation is dependent on duration of pressure reduction. Removal of the endothelium caused partial inhibition of this dilation. We sought to determine which of three endothelium mediated signals, hyperpolarization, nitric oxide, or prostacyclin were involved in myogenic and reactive dilation. Rat soleus feed arteries were isolated and cannulated for in vitro videomicroscopic observation. To induce reactive dilation, intraluminal pressure was reduced from 115 cmH2O to 14 cmH2O for 2 min periods followed by a return to 115 cmH2O in the presence of various blockers. A combination of 20 mM K+ (membrane potential “clamp”) and 0.01 mM indomethacin (prostaglandin inhibitor) (N=4), and a combination of 20 mM K+, 0.01 mM indomethacin, and 0.3 mM nitroarginine (nitric oxide inhibitor) failed to inhibit dilation (N=6) (max: 53.3±4.6%, inhibited: 60.0±32.1% and max: 45.3±8.4%, inhibited: 75.9±37.9%, respectively). The myogenic protocol consisted of a sustained increase in pressure from a baseline of 80 cmH2O to 135 cmH2O in the presence of same blockers. Arteries dilated to the sustained pressure increase, and no inhibition of dilation was seen with the combination of 20 mM K+ and 0.3 mM nitroarginine (N=3) (30.0±2.9%, inhibited: 47.1±24.0%). However, inhibition of dilation was seen with the combination of 20 mM K+, 0.3 mM nitroarginine , and 0.01 mM indomethacin (N=3) (max: 34.8±8.7%, inhibited: 10.2±3.1%). These data suggest that reactive dilation is not dependent on membrane hyperpolarization, nitric oxide or prostacyclin, but myogenic dilation is partially dependent on prostacyclin. Thus reactive and myogenic dilation utilize different mechanisms.