Arteriolar response to sympathetic stimulation in skeletal muscle is highly dependent on vessel location within the network and is modulated by local oxygen levels.
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Local O2 modulates sympathetic escape in animal skeletal muscle arterioles; leaves open translation to human perfusion under hypoxia.
The influence of vessel location on arteriolar responses to sympathetic nerve stimulation was systematically studied in a skeletal muscle arteriolar network under normal and altered tissue O2 levels. The exteriorized cat sartorius muscle was exposed to 0, 5, and 10% ambient O2 during sympathetic chain stimulation at 8 pulses/s. Under 0% O2, stimulation initially caused a 25-45% constriction that was faster and more pronounced in distal arterioles. Ninety-one percent of vessels showed a secondary dilation (sympathetic escape), which was largest in distal arterioles. Escape had little effect on calculated volume flow, which, after a large initial fall, showed a modest secondary increase. Under 5 and 10% O2, resting arteriolar diameter was reduced by 12 and 17%, respectively, and escape was reduced by 60 and 73%. Escape was not attenuated in proximal arterioles preconstricted with vasopressin, suggesting that O2 did not attenuate escape through increased vascular tone. Therefore, the arteriolar response to sympathetic stimulation depends largely on location within the network and is modulated to varying degrees by metabolic influences.
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Boegehold et al. (1988) studied this question.
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