The effect of shear stress, potassium, and adenosine on α-1 adrenergic vasoconstriction of rat soleus feed arteries

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\u27s research poster

Harvey Newton Heckle Papers - Accession 282

Harvey Newton Heckle (1902-1979) was a clubman and worked with the South Carolina Highway Department as the state’s District 4 engineer. The Harvey Newton Heckle Papers consist of correspondence, memoranda, reports, newspaper clippings, and handwritten notes pertaining to Heckle’s activities with the South Carolina Highway Department as the state’s District 4 engineer. Mr. Heckle’s work with the First Baptist Church of Chester, the Lion’s Club, the Exchange Club, and the Chester County Historical Society is also well documented. The collection also includes records pertaining to A.M. Heckle’s, Harvey’s uncle, work with the Southern Railway in Macon, Georgia and Amelia Heckle, Harvey’s daughter, which includes certificates, educational brochures, and correspondence.https://digitalcommons.winthrop.edu/manuscriptcollection_findingaids/1306/thumbnail.jp

The Effect of Shear Stress, Potassium, and Adenosine on α-1 Adrenergic Vasoconstriction of Rat Soleus Feed Arteries

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

Beekeeping adoption : A case study of three smallholder farming communities in Baringo County, Kenya

Peer reviewedPublisher PD

Mechanism of nitric oxide induced sympatholysis in rat soleus feed arteries

During exercise, the neurotransmitter norepinephrine (NE) binds to arterial adrenergic receptors to cause vasoconstriction, yet arteries and arterioles constrict less to sympathetic stimulation in contracting compared to resting skeletal muscle (sympatholysis). Previous evidence indicates that nitric oxide (NO) can be sympatholytic, but the mechanism is unknown. We hypothesized that NO causes sympatholysis in rat soleus muscle feed arteries, that NO is released from vascular endothelial cells by increased shear stress, and that NO acts through a guanylyl cyclase intracellular signaling pathway. 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 adrenergic agonist phenylephrine (PE; 10-9 M to 10-4 M, 0.5 log increments) in the presence of varying levels of the nitric oxide donor sodium nitroprusside (SNP; 0 nM, 0.1 nM and 100 nM), shear stress (0 dy/cm2, 25 dy/cm2, and 135 dy/cm2), and SNP + ODQ (0.1 nM), an inhibitor of guanylyl cyclase. SNP reduced constriction to PE in a dose-dependent manner (maximum constriction 77.3 % vs. 70.7 % and 56.7 %), indicating that NO interferes with sympathetic constriction. ODQ restored PE-induced constriction (PE alone 77.5%; with SNP 67.6%; with SNP + ODQ 83.5%), indicating that NO causes sympatholysis through a guanylyl cyclase signaling pathway. However, shear stress did not reduce constriction to PE (67.6 % vs. 68.1 %, and 67.6 %), indicating that increased shear stress during exercise is not the source of the NO causing sympatholysis. We conclude that nitric oxide acting through guanylyl cyclase causes sympatholysis, but the source of the nitric oxide during exercise is not shear stress-induced endothelial cell activation

La Golondrina

Illustration of swallows flying with birdhouse on post in backgroundhttps://scholarsjunction.msstate.edu/cht-sheet-music/8016/thumbnail.jp