Document Type

Research Poster

Publication Date

Summer 2013

Abstract

During exercise, blood flow increases to the working skeletal muscle primarily because of dilation of the arteries and arterioles feeding the muscle. Sympathetic nerve activity also increases during exercise, augmenting the release of the neurotransmitter norepinephrine (NE) at the arterial wall and into the blood. NE acts to constrict blood vessels; however, arteries and arterioles within contracting skeletal muscle dilate despite the increased NE present. This has led to the concept of functional sympatholysis (4), the idea that a chemical released from contracting skeletal muscle interferes with NE signaling. NE acts by binding to adrenergic (alpha and beta) receptors, and it is alpha receptors in the arterial wall that cause vasoconstriction (8). While both α-1 and α-2 receptor subtypes have been found in some vascular beds of some species, there is significant evidence that in rat calf muscles, the response to norepinephrine is mediated solely by α-1 receptors (5, 9). Because α-1 receptors are the sole respondents to sympathetic signaling, we studied three proposed substances that may interfere with sympathetic signaling at the α-1 receptors, thereby mediating sympatholysis. There is evidence to suggest that heat and acidosis may partially mediate sympatholysis of α-1 receptors (1, 2). This study sought to determine whether increased levels of shear stress, potassium, or adenosine also contribute to sympatholysis. If shear stress, potassium, and adenosine are, in fact, sympatholytic agents, they will reduce the vasoconstriction mediated by the α-1 receptors in rat soleus muscle feed arteries. We hypothesized that all three variables would be sympatholytic agents.

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