The effect of shear stress, potassium, adenosine, and acidosis on alpha‐1 adrenergic vasoconstriction of rat soleus feed arteries (1170.14)

Abstract

Arteries and arterioles constrict less to sympathetic stimulation in contracting compared to resting skeletal muscle (sympatholysis). There is some uncertainty regarding the specific agents causing sympatholysis. We hypothesized that increased levels of arterial wall shear stress, potassium, adenosine, or acidosis contribute to sympatholysis, thereby reducing sympathetic vasoconstriction. Soleus feed arteries (n = 12 per group) were isolated from male Sprague‐Dawley rats and cannulated on two glass micropipettes for in vitro videomicroscopy. We measured the constriction response to the α‐1 agonist phenylephrine (PE; 10‐9 M to 10‐4 M, 0.5 log increments) in the presence of varying levels of shear stress (0 dy/cm2, 25 dy/cm2, and 135 dy/cm2), potassium (5 mM, 7.5 mM, and 10 mM), adenosine (0 μM, 0.8 μM, and 1.6 μM) and acidosis (pH = 7.4, 7.1, 6.8, and 6.5). There was no significant difference in PE induced constriction between levels of shear stress (maximum constriction 67.6 % vs. 68.1 % and 67.6 %), potassium (maximum constriction 63.1 % vs. 56.5 % and 65.0 %), or adenosine (maximum constriction 56.2 % vs. 54.3 % and 54.2 %). However, acidosis reduced constriction to PE (maximum constriction 77.6% vs. 72.0%, 66.6%, and 66.3%). We conclude that acidity, but not shear stress, potassium, or adenosine, is sympatholytic in feed arteries from the predominantly slow twitch soleus muscle.Grant Funding Source: Supported by NSF #DBI‐1062721 and the Seaver Research Council