Myogenic Constriction
Myogenic Constriction - Related Videos
13:43
Fabrication of Myogenic Engineered Tissue Constructs
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Cited by 11 •
2009
Here, we demonstrate fabrication of collagen-based, tissue constructs containing skeletal myoblasts. These 3-D engineered constructs may be used to replace or repair tissues in vivo. For our purposes, we have designed these as an atrioventricular electrical conduit for the repair of complete heart block[1].
08:25
Transverse Aortic Constriction in Mice
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Cited by 263 •
2010
Transverse aortic constriction (TAC) in the mouse is a commonly used experimental model to study mechanisms underlying cardiac hypertrophy and heart failure development. Here, we describe procedures to constrict the aorta to create a reproducible degree of cardiac hypertrophy in mice.
10:48
Assessing Myogenic Response and Vasoactivity In Resistance Mesenteric Arteries Using Pressure Myography
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Cited by 24 •
2015
Pressure myography is used to assess vasoactivity of small arteries that develop sustained constriction when pressurized. This manuscript provides a detailed protocol to assess in isolated segments of small mesenteric arteries from rats, vasoactivity and the effect of intraluminal pressure on vascular diameter.
07:40
Minimally Invasive Transverse Aortic Constriction in Mice
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Cited by 42 •
2017
Minimally invasive transverse aortic constriction (MTAC) conserves the essentials of regular transverse aortic constriction (TAC) while eliminating the use of a ventilator with tracheal intubation. It proves to be a highly desirable method for high-throughput studies on left ventricular overload, particularly in translational studies.
07:51
Preparation of Primary Myogenic Precursor Cell/Myoblast Cultures from Basal Vertebrate Lineages
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Cited by 32 •
2014
In vitro culture systems have proven indispensible to our understanding of vertebrate myogenesis. However, much remains to be learned about nonmammalian skeletal muscle development and growth, particularly in basal taxa. An efficient and robust protocol for isolating the adult stem cells of this tissue, the myogenic precursor cells (MPCs), and maintaining their self-renewal, proliferation, and differentiation in a primary culture setting allows for the identification of conserved and divergent...
FAQs
Stretch activates mechanosensitive signaling in the vascular smooth-muscle cells, which depolarizes their membrane. This electrical change opens voltage-gated calcium channels, allowing calcium to enter the cells. Calcium then activates the contractile machinery formed by actin and myosin. The sequence links a mechanical pressure change to active narrowing of the vessel and increased vascular resistance.
Calcium entry converts membrane depolarization into mechanical contraction. After stretch-associated signaling opens voltage-gated calcium channels, the incoming calcium activates actin-myosin interactions within vascular smooth muscle. Without this coupling step, the pressure stimulus would not efficiently produce vessel narrowing. Calcium therefore serves as the key intracellular signal connecting mechanosensation with the resistance change that influences blood flow.
Myogenic constriction begins with a mechanical stimulus, specifically increased intraluminal pressure and smooth-muscle stretch. In inflammatory settings, endothelial signals and inflammatory mediators can modify the resulting vessel tone. Thus, the response has an intrinsic pressure-sensitive component but does not operate in isolation. Infection or inflammation may alter how the microvasculature regulates resistance and perfusion.
Intraluminal pressure provides the mechanical input that activates the smooth-muscle response. As pressure stretches the vessel wall, mechanosensitive signaling promotes membrane depolarization, calcium influx, and contraction. The resulting increase in vascular resistance helps stabilize tissue blood flow despite pressure changes. This pressure-flow relationship is central to understanding autoregulation in the microcirculation.
Researchers can examine how pressure-related smooth-muscle responses affect vascular resistance, tissue perfusion, and pressure-flow autoregulation. The response also provides a framework for considering downstream consequences for tissue oxygen delivery. Comparing these relationships under baseline and inflammatory conditions can reveal how endothelial signals or inflammatory mediators modify microvascular tone, without treating pressure regulation as an isolated process.
Inflammation and infection can change the signals that regulate microvascular tone. Because myogenic constriction contributes to pressure-flow control, such changes may influence local perfusion and oxygen delivery in affected tissues. Studying this interaction helps connect vascular smooth-muscle behavior with inflammatory vascular dysfunction and clarifies how altered vessel regulation may shape tissue responses during infectious disease.
Analysis of myogenic constriction can help explain altered tissue perfusion, disrupted oxygen delivery, and vascular dysfunction associated with infectious or inflammatory disease. The relevant interpretation links pressure sensing, calcium-dependent smooth-muscle contraction, and changes in vascular resistance. These outcomes show why microvascular tone is important when evaluating how disease-related signals affect circulation within tissues.