Presentation Type
Oral Presentation
Keywords
Science, biology, Human Physiology, exercise, shear stress, arteries and arterioles, sympathetic signaling
Department
Sports Medicine
Major
Sports Medicine
Abstract
During exercise, sympathetic nerve activity increases, augmenting the release of the neurotransmitter norepinephrine (NE) at the arterial wall and into the blood. NE binds to arterial adrenergic receptors to cause vasoconstriction, yet arteries in contracting skeletal muscle dilate during exercise. Previous evidence from Ives et al. suggests that heat and acidosis may partially inhibit constriction resulting from α-1 adrenergic receptors (termed sympatholysis). Our lab has previously demonstrated that rat soleus feed arteries respond to sympathetic signaling solely by α-1 adrenoceptors. We hypothesized that increased levels of arterial wall shear stress, potassium, or adenosine also contribute to sympatholysis, thereby reducing sympathetic vasoconstriction. This study measured the constriction response to phenylephrine (PE; an α-1 agonist) in the presence of varying levels of shear stress, potassium, and adenosine. Soleus feed arteries were isolated from male Sprague-Dawley rats and cannulated on two glass micropipettes for in vitro video microscopy. PE dose-response curves (10−9 M to 10−4 M, 0.5 log increments) were evaluated for shear stress (0 dy/cm2, 25 dy/cm2, and 135 dy/cm2), potassium (5 mM, 7.5 mM, and 10 mM), and adenosine (0 μM, 0.8 μM, and 1.6 μM). We found that the three proposed sympatholytic agents did not reduce vasoconstriction to phenylephrine (n = 12 rats per group). There was no significant difference between the constriction for each level of shear stress (maximum constriction 71.8 %, 71.6 %, 69.4 %), potassium (maximum constriction 67.8 %, 62.8 %, 68.5 %), and adenosine (maximum constriction 59.8 %, 60.2 %, 57.2 %), respectively. We conclude that the predominantly slow twitch soleus muscle may not be capable of fighting sympathetic vasoconstriction, and we are pursuing these same studies in the mixed fiber type rat gastrocnemius.
See also author's research poster.
Faculty Mentor
Jeffrey Jasperse
Funding Source or Research Program
Academic Year Undergraduate Research Initiative, Summer Undergraduate Research in Biology
Presentation Session
Session E
Location
Rockwell Academic Center 178
Start Date
21-3-2014 4:00 PM
Included in
The effect of shear stress, potassium, and adenosine on α-1 adrenergic vasoconstriction of rat soleus feed arteries
Rockwell Academic Center 178
During exercise, sympathetic nerve activity increases, augmenting the release of the neurotransmitter norepinephrine (NE) at the arterial wall and into the blood. NE binds to arterial adrenergic receptors to cause vasoconstriction, yet arteries in contracting skeletal muscle dilate during exercise. Previous evidence from Ives et al. suggests that heat and acidosis may partially inhibit constriction resulting from α-1 adrenergic receptors (termed sympatholysis). Our lab has previously demonstrated that rat soleus feed arteries respond to sympathetic signaling solely by α-1 adrenoceptors. We hypothesized that increased levels of arterial wall shear stress, potassium, or adenosine also contribute to sympatholysis, thereby reducing sympathetic vasoconstriction. This study measured the constriction response to phenylephrine (PE; an α-1 agonist) in the presence of varying levels of shear stress, potassium, and adenosine. Soleus feed arteries were isolated from male Sprague-Dawley rats and cannulated on two glass micropipettes for in vitro video microscopy. PE dose-response curves (10−9 M to 10−4 M, 0.5 log increments) were evaluated for shear stress (0 dy/cm2, 25 dy/cm2, and 135 dy/cm2), potassium (5 mM, 7.5 mM, and 10 mM), and adenosine (0 μM, 0.8 μM, and 1.6 μM). We found that the three proposed sympatholytic agents did not reduce vasoconstriction to phenylephrine (n = 12 rats per group). There was no significant difference between the constriction for each level of shear stress (maximum constriction 71.8 %, 71.6 %, 69.4 %), potassium (maximum constriction 67.8 %, 62.8 %, 68.5 %), and adenosine (maximum constriction 59.8 %, 60.2 %, 57.2 %), respectively. We conclude that the predominantly slow twitch soleus muscle may not be capable of fighting sympathetic vasoconstriction, and we are pursuing these same studies in the mixed fiber type rat gastrocnemius.
See also author's research poster.