Regulation of in situ skeletal muscle arteriolar tone: interactions between two parameters.
OBJECTIVE
The growing understanding of the complexity of mechanisms regulating arteriolar tone demands that a systematic determination of how these processes interact to alter diameter be undertaken. This study examined how five mediators of skeletal muscle distal arteriolar tone [adenosine concentration, oxygen content, alpha-adrenergic activation (norepinephrine), intravascular pressure and wall shear rate], taken two parameters at a time, interact to regulate vessel diameter.


METHODS
The reactivity of distal arterioles of in situ rat cremaster muscle after alterations in each of the above mediators was assessed. In addition, arteriolar responses to all two-parameter combinations were evaluated to determine the effect of altered environment on vascular reactivity to stimuli.


RESULTS
Arteriolar dilation to adenosine was unaltered by changes in other parameters. In contrast, wall shear rate-induced arteriolar dilation was impaired by 60-88% after increases in the other parameters. Myogenic reactivity was reduced by 28% with elevated O(2) and by 65% with norepinephrine (because of vessel closure) and was impaired by 89% with elevated adenosine. O(2)-induced arteriolar reactivity was impaired by 56% with increased adenosine and by 44% with increased norepinephrine concentration but was largely unaffected by elevated intravascular pressure. Adrenergic reactivity was attenuated with elevated intravascular pressure (by 69%) and O(2) (by 54%) because of vessel closure but was unaltered with elevated adenosine.


CONCLUSIONS
These data suggest that (1) individual mediators contributing to the regulation of arteriolar tone exist within a hierarchy of importance and (2) mechanisms regulating arteriolar tone can be impacted by unidentified alterations in other processes. Ongoing investigation into interactions between multiple processes regulating arteriolar tone will allow for a more integrated understanding of how microvessels regulate their diameter.
Frisbee
Jefferson C
JC
Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. jfrisbee@mcw.edu
D000241:Adenosine / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D008297:Male; D018715:Microscopy, Video; D018482:Muscle, Skeletal / Q000098:blood supply*; D010100:Oxygen / Q000494:pharmacology; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
D000316:Adrenergic alpha-Agonists; D000241:Adenosine; D010100:Oxygen