GO:0014826 vein smooth muscle contraction: Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0014826 vein smooth muscle contraction describes the force-generating process within venous smooth muscle that changes muscle geometry, driven by actin/myosin ATP hydrolysis.
• Venous smooth muscle contraction is activated by neurohumoral agents including endothelin via ETA and ETB receptors and by neurokinin-2 receptor stimulation in human saphenous veins.
• Mechanical and pharmacological studies show that vein contraction can cause endothelial damage during graft preparation, linking this process to vascular injury.
• Anesthetics such as urethane and pentobarbital modulate vascular smooth muscle contraction, indicating that venous tone is sensitive to pharmacological agents.
• Ajmaline alters contraction patterns of portal vein smooth muscle strips, demonstrating that ion channel-active drugs can directly influence venous contractility.
• Minimally invasive saphenous vein harvesting affects endothelial and smooth muscle function, making vein contraction a clinically relevant research target in cardiovascular surgery.
Description
GO:0014826 vein smooth muscle contraction is a biological process in which force is generated within smooth muscle tissue of the vein, resulting in a change in muscle geometry. This process depends on chemo-mechanical energy conversion carried out by the actin/myosin complex, which generates force through ATP hydrolysis. The vein is a vessel that carries blood away from the capillary beds, and its smooth muscle layer provides the contractile machinery that regulates venous capacitance and return. Understanding this process is important because venous smooth muscle contraction contributes to vascular tone, graft preparation injury, and responses to pharmacological agents. Experimental studies have shown that vein contraction and smooth muscle cell extensions can cause endothelial damage during graft preparation, highlighting the clinical relevance of this process. In addition, isolated portal vein smooth muscle strips respond to drugs such as ajmaline, providing a model for studying contraction patterns in venous tissue. Neurohumoral regulation of venous smooth muscle involves specific receptors, including endothelin ETA and ETB receptors and neurokinin-2 receptors in human saphenous veins. These findings establish vein smooth muscle contraction as a tractable and medically important process for cardiovascular and pharmacological research.
vein smooth muscle contraction At A Glance
| GO ID | GO:0014826 |
|---|---|
| GO term | vein smooth muscle contraction |
| Ontology | biological_process |
| Synonym | None |
| Major function | Force generation within venous smooth muscle tissue via actin/myosin ATP hydrolysis, resulting in a change in muscle geometry |
| Anatomical location | Vein, a vessel carrying blood away from the capillary beds |
| Key molecular machinery | Actin/myosin complex |
| Energy source | ATP hydrolysis |
| Regulatory receptors | Endothelin ETA and ETB receptors; neurokinin-2 receptors |
What Is GO:0014826?
GO:0014826 vein smooth muscle contraction is defined as a process in which force is generated within smooth muscle tissue of the vein, resulting in a change in muscle geometry. The force generation involves a chemo-mechanical energy conversion step carried out by the actin/myosin complex, which generates force through ATP hydrolysis. The vein is a vessel carrying blood away from the capillary beds, and its smooth muscle contraction is distinct from arterial or other smooth muscle contraction in its anatomical location and functional context.
Why Is vein smooth muscle contraction Important in Cell Biology?
Vein smooth muscle contraction is important because it regulates venous capacitance and blood return, and its dysregulation or mechanical consequences can lead to endothelial damage during graft preparation. Pharmacological modulation of venous smooth muscle contraction by agents such as urethane, pentobarbital, and ajmaline demonstrates that this process is a target for drug action and a determinant of vascular reactivity. Receptor-mediated contraction via endothelin ETA/ETB and neurokinin-2 receptors in human saphenous veins further links this process to neurohumoral control of venous tone. Surgical harvesting techniques also affect endothelial and smooth muscle function, making vein smooth muscle contraction a clinically relevant endpoint in cardiovascular procedures.
• Venous smooth muscle contraction regulates venous capacitance and blood return to the heart.
• Excessive vein contraction during graft preparation can cause endothelial damage, affecting graft quality.
• Endothelin ETA and ETB receptors mediate vascular smooth muscle contraction, including in venous tissue.
• Neurokinin-2 receptors mediate contraction in human saphenous veins, linking tachykinin signaling to venous tone.
• Anesthetics such as urethane and pentobarbital modulate vascular smooth muscle contraction, relevant to experimental and clinical pharmacology.
• Ajmaline alters contraction patterns of portal vein smooth muscle strips, showing drug effects on venous contractility.
• Minimally invasive saphenous vein harvesting affects endothelial and smooth muscle function, a surgical quality issue.
• Ultrastructural studies of vascular smooth muscle activation provide a basis for understanding contraction mechanisms.
• Vein smooth muscle contraction is a model process for studying chemo-mechanical energy conversion by actin/myosin.
• Pharmacological modulation of venous contraction has implications for cardiovascular drug development.
What Happens During vein smooth muscle contraction?
Activation and force generation
In simple terms: The vein's smooth muscle cells receive a signal and start to pull, generating force.
Vein smooth muscle contraction is a process in which force is generated within smooth muscle tissue, resulting in a change in muscle geometry. Force generation involves a chemo-mechanical energy conversion step carried out by the actin/myosin complex, which generates force through ATP hydrolysis. Ultrastructural aspects of activation and contraction of vascular smooth muscle have been described, providing a structural basis for this process.
Receptor-mediated activation
In simple terms: Signaling molecules bind to receptors on the vein muscle cells and trigger contraction.
Endothelin ETA and ETB receptors mediate vascular smooth muscle contraction, including in venous preparations. In human saphenous veins, smooth muscle neurokinin-2 receptors mediate contraction, demonstrating receptor-specific control of venous tone.
Pharmacological modulation
In simple terms: Drugs can change how strongly or how often the vein muscle contracts.
Urethane and pentobarbital modulate contraction of vascular smooth muscle, indicating that venous contractility is sensitive to anesthetic agents. Ajmaline affects contraction patterns of isolated rat portal vein smooth muscle strips, further showing that pharmacological agents can directly alter venous contraction.
Mechanical consequences and endothelial damage
In simple terms: When the vein muscle contracts strongly, it can injure the inner lining of the vein.
Vein contraction and smooth muscle cell extensions can cause endothelial damage during graft preparation, linking the contractile process to vascular injury. Minimally invasive saphenous vein harvesting also affects endothelial and smooth muscle function, underscoring the clinical relevance of vein contraction and its modulation.
Key Genes Involved in GO:0014826 vein smooth muscle contraction
The following genes and proteins are experimentally implicated in vein smooth muscle contraction or its pharmacological modulation, based on the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| EDNRA | Endothelin ETA receptor mediates vascular smooth muscle contraction | Target for studying endothelin-driven venous contraction |
| EDNRB | Endothelin ETB receptor mediates vascular smooth muscle contraction | Target for studying endothelin-driven venous contraction |
| TACR2 | Neurokinin-2 receptor mediates contraction in human saphenous veins | Target for tachykinin-mediated venous contraction |
| MYH11 | Smooth muscle myosin heavy chain, part of the actin/myosin complex generating force via ATP hydrolysis | Core contractile machinery for vein smooth muscle contraction |
| ACTA2 | Smooth muscle actin, part of the actin/myosin complex generating force | Core contractile machinery for vein smooth muscle contraction |
| MYLK | Myosin light chain kinase regulates smooth muscle contraction | Regulatory node for actin/myosin activation |
| MYL9 | Myosin regulatory light chain, regulates smooth muscle contraction | Regulatory node for actin/myosin activation |
| CALD1 | Caldesmon regulates smooth muscle contraction | Regulatory node for actin/myosin activation |
| CNN1 | Calponin regulates smooth muscle contraction | Regulatory node for actin/myosin activation |
| ATP2B1 | Plasma membrane calcium ATPase influences calcium handling in smooth muscle | Calcium regulation in vein smooth muscle |
| SCN5A | Voltage-gated sodium channel modulated by ajmaline in smooth muscle strips | Drug response studies in portal vein smooth muscle |
| KCNMA1 | Large-conductance calcium-activated potassium channel influences smooth muscle tone | Ion channel modulation of venous contraction |
| GJA1 | Connexin 43 contributes to smooth muscle cell communication | Cell-to-cell coupling in vascular smooth muscle |
| NOS3 | Endothelial nitric oxide synthase modulates vascular smooth muscle tone | Endothelial-smooth muscle interaction in vein grafts |
| PTGS2 | Cyclooxygenase-2 influences vascular smooth muscle contraction | Pharmacological modulation of venous contraction |
| ADORA2A | Adenosine receptor influences vascular smooth muscle contraction | Anesthetic modulation of venous contraction |
| CACNA1C | Voltage-gated calcium channel contributes to smooth muscle contraction | Calcium entry in vein smooth muscle |
| ROCK1 | Rho-associated kinase regulates smooth muscle contraction | Calcium sensitization in vein smooth muscle |
How Is vein smooth muscle contraction Regulated?
Vein smooth muscle contraction is regulated by receptor-mediated signaling, including endothelin ETA and ETB receptors and neurokinin-2 receptors in human saphenous veins. Pharmacological agents such as urethane, pentobarbital, and ajmaline modulate contraction of vascular or portal vein smooth muscle, indicating that anesthetic and antiarrhythmic drugs can influence this process. Endothelial function also modulates venous smooth muscle behavior, as shown by the effects of minimally invasive saphenous vein harvesting on endothelial and smooth muscle function.
vein smooth muscle contraction and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| EDNRA | Vascular tone dysregulation | Knockout or point-mutation in venous smooth muscle cells |
| EDNRB | Vascular tone dysregulation | Knockout or point-mutation in venous smooth muscle cells |
| TACR2 | Venous contraction abnormalities | Knockout in human saphenous vein smooth muscle cells |
| NOS3 | Endothelial dysfunction in vein grafts | Overexpression or knockout in vein endothelial cells |
| MYH11 | Smooth muscle contractile dysfunction | Point mutation or knockout in smooth muscle cells |
Vein graft injury and endothelial damage
Vein contraction and smooth muscle cell extensions can cause endothelial damage during graft preparation, which is relevant to coronary artery bypass grafting and other vascular surgeries. Minimally invasive saphenous vein harvesting also affects endothelial and smooth muscle function, further linking vein smooth muscle contraction to graft quality and clinical outcomes.
Vascular tone dysregulation and pharmacological responses
Endothelin ETA and ETB receptors mediate vascular smooth muscle contraction, and their activity in veins contributes to vascular tone regulation. Neurokinin-2 receptors mediate contraction in human saphenous veins, suggesting that tachykinin signaling may be involved in venous tone abnormalities. Anesthetics such as urethane and pentobarbital modulate vascular smooth muscle contraction, which has implications for patients undergoing surgery.
Drug effects on venous contractility
Ajmaline affects contraction patterns of isolated rat portal vein smooth muscle strips, indicating that antiarrhythmic drugs can directly alter venous contractility. This has potential implications for understanding drug effects on venous return and portal circulation.
From vein smooth muscle contraction-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does EDNRA mediate vein smooth muscle contraction? | EDNRA knockout in venous smooth muscle cells |
| Does TACR2 mediate human saphenous vein contraction? | TACR2 knockout in human saphenous vein smooth muscle cells |
| Does ajmaline alter portal vein contraction patterns? | Point mutation in ion channel genes in portal vein smooth muscle cells |
| Does NOS3 modulate vein graft endothelial-smooth muscle function? | NOS3 overexpression in vein endothelial cells |
| Does MYH11 ATP hydrolysis drive vein smooth muscle force? | MYH11 point mutation in smooth muscle cells |
| Does urethane modulate vascular smooth muscle contraction? | Knockout of anesthetic-sensitive pathways in vascular smooth muscle cells |
How to Study the vein smooth muscle contraction Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Isolated smooth muscle strip assay | Force generation and contraction patterns | Drug effects on portal vein contraction |
| Receptor pharmacology | Agonist/antagonist effects on contraction | Endothelin and neurokinin receptor studies |
| Ultrastructural imaging | Structural changes during activation | Vascular smooth muscle contraction mechanism |
| Graft preparation injury assessment | Endothelial damage from vein contraction | Vein graft quality studies |
| Saphenous vein harvesting functional test | Endothelial and smooth muscle function | Minimally invasive harvesting outcomes |
| Anesthetic modulation assay | Effect of urethane/pentobarbital on contraction | Vascular smooth muscle pharmacology |
| Ion channel drug response | Contraction pattern changes with ajmaline | Portal vein smooth muscle studies |
Isolated smooth muscle strip contractility assays
Isolated rat portal vein smooth muscle strips have been used to study contraction patterns and the effects of drugs such as ajmaline. Similar strip preparations from vascular smooth muscle allow direct measurement of force generation and pharmacological responses.
Receptor pharmacology and agonist/antagonist studies
Endothelin ETA and ETB receptor-mediated contraction has been characterized in vascular smooth muscle using pharmacological tools. Neurokinin-2 receptor-mediated contraction in human saphenous veins has been demonstrated with selective agonists and antagonists.
Ultrastructural and imaging approaches
Ultrastructural aspects of activation and contraction of vascular smooth muscle have been studied to understand the structural basis of force generation. Vein contraction and smooth muscle cell extensions have been visualized in the context of endothelial damage during graft preparation.
Surgical and functional assessment of vein grafts
Minimally invasive saphenous vein harvesting has been assessed for its effects on endothelial and smooth muscle function, providing a clinical method to evaluate vein contraction-related outcomes.
How CRISPR Can Be Used to Study GO:0014826 vein smooth muscle contraction
Knockout
CRISPR knockout of EDNRA, EDNRB, or TACR2 in venous smooth muscle cells can test whether these receptors are required for vein smooth muscle contraction. Knockout of MYH11 or ACTA2 can disrupt the core actin/myosin contractile machinery.
Point Mutation
Point mutations in ion channel genes such as SCN5A or KCNMA1 can model altered responses to drugs like ajmaline in portal vein smooth muscle. Point mutations in MYH11 can probe ATP hydrolysis-dependent force generation.
Knock-in
Knock-in of tagged contractile proteins such as MYH11 or ACTA2 can enable live-cell imaging of the actin/myosin complex during vein smooth muscle contraction. Knock-in of reporter alleles for EDNRA or TACR2 can track receptor expression in venous tissue.
Overexpression
Overexpression of NOS3 in vein endothelial cells can test its modulatory role in endothelial-smooth muscle function. Overexpression of contractile or regulatory proteins can enhance or suppress vein smooth muscle contraction in vitro.
How EDITGENE Supports vein smooth muscle contraction Research
Researchers studying vein smooth muscle contraction-related genes often need to determine whether a candidate gene is causally involved in force generation, receptor-mediated activation, or pharmacological modulation. EDITGENE provides CRISPR-based cell model services to support such mechanistic studies in venous smooth muscle and endothelial cells.
Contact EDITGENE today to design your custom CRISPR model for vein smooth muscle contraction research.
Frequently Asked Questions About vein smooth muscle contraction
What is GO:0014826 vein smooth muscle contraction?
GO:0014826 is a biological process in which force is generated within smooth muscle tissue of the vein, resulting in a change in muscle geometry, driven by actin/myosin ATP hydrolysis.
What genes are involved in vein smooth muscle contraction?
Genes experimentally implicated include EDNRA and EDNRB (endothelin receptors), TACR2 (neurokinin-2 receptor), and contractile machinery genes such as MYH11 and ACTA2.
How is vein smooth muscle contraction regulated?
It is regulated by receptor-mediated signaling, including endothelin ETA/ETB and neurokinin-2 receptors, and is modulated by pharmacological agents such as urethane, pentobarbital, and ajmaline.
Why is vein smooth muscle contraction important in surgery?
Vein contraction and smooth muscle cell extensions can cause endothelial damage during graft preparation, and harvesting techniques affect endothelial and smooth muscle function.
What receptors mediate vein smooth muscle contraction?
Endothelin ETA and ETB receptors mediate vascular smooth muscle contraction, and neurokinin-2 receptors mediate contraction in human saphenous veins.
Can drugs affect vein smooth muscle contraction?
Yes, urethane and pentobarbital modulate vascular smooth muscle contraction, and ajmaline alters contraction patterns of isolated rat portal vein smooth muscle strips.
What is the role of the actin/myosin complex in vein smooth muscle contraction?
The actin/myosin complex carries out chemo-mechanical energy conversion and generates force through ATP hydrolysis during vein smooth muscle contraction.
How do researchers study vein smooth muscle contraction?
Methods include isolated smooth muscle strip assays, receptor pharmacology, ultrastructural imaging, and functional assessment of vein grafts.
What is the definition of vein smooth muscle contraction according to QuickGO?
It is a process in which force is generated within smooth muscle tissue, resulting in a change in muscle geometry, occurring in the vein and involving actin/myosin ATP hydrolysis.
Which model systems are used for vein smooth muscle contraction research?
Isolated rat portal vein smooth muscle strips and human saphenous vein preparations are used, along with pharmacological and ultrastructural methods.
Conclusion
GO:0014826 vein smooth muscle contraction is a biologically and clinically significant process in which venous smooth muscle generates force through actin/myosin ATP hydrolysis, leading to changes in muscle geometry. Experimental evidence links this process to receptor-mediated signaling by endothelin and neurokinin-2 receptors, pharmacological modulation by anesthetics and antiarrhythmic drugs, and endothelial damage during vein graft preparation. Understanding the mechanisms and regulation of vein smooth muscle contraction can inform cardiovascular research, surgical practice, and drug development. CRISPR-based cell models provide a powerful approach to dissect the causal roles of specific genes in this process.
References
- 1. Baumann FG et al.. 1981. Vein contraction and smooth muscle cell extensions as causes of endothelial damage during graft preparation.. Ann Surg 194(2):199-211 PMID: 7259348
- 2. Patejdl R et al.. 2019. Effects of ajmaline on contraction patterns of isolated rat gastric antrum and portal vein smooth muscle strips and on neurogenic relaxations of gastric fundus.. Pflugers Arch 471(7):995-1005 PMID: 31044280
- 3. Somlyo AP et al.. 1976. Ultrastructural aspects of activation and contraction of vascular smooth muscle.. Fed Proc 35(6):1288-93 PMID: 770202
- 4. Altura BM et al.. 1979. Urethane and contraction of vascular smooth muscle.. Br J Pharmacol 67(2):255-63 PMID: 497529
- 5. Mechiche H et al.. 2011. Smooth muscle neurokinin-2 receptors mediate contraction in human saphenous veins.. Pharmacol Res 63(5):414-22 PMID: 21272642
- 6. Black EA et al.. 2001. Minimally invasive saphenous vein harvesting: effects on endothelial and smooth muscle function.. Ann Thorac Surg 71(5):1503-7 PMID: 11383790
- 7. Altura BT et al.. 1975. Pentobarbital and contraction of vascular smooth muscle.. Am J Physiol 229(6):1635-40 PMID: 1211497
- 8. Sumner MJ et al.. 1992. Endothelin ETA and ETB receptors mediate vascular smooth muscle contraction.. Br J Pharmacol 107(3):858-60 PMID: 1472978
