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The endothelium and its role in regulating vascular tone.

Sandoo A, van Zanten JJ, Metsios GS, Carroll D, Kitas GD - Open Cardiovasc Med J (2010)

Bottom Line: The endothelium forms an important part of the vasculature and is involved in promoting an atheroprotective environment via the complementary actions of endothelial cell-derived vasoactive factors.The present review aims to provide an insight into the anatomy of the vasculature as well as the underlying endothelial cell physiology.In addition, an in-depth overview of the current methods used to assess vascular function and structure is provided as well as their link to certain clinical populations.

View Article: PubMed Central - PubMed

Affiliation: School of Sport and Exercise Sciences, University of Birmingham, Birmingham, West Midlands, United Kingdom.

ABSTRACT
The endothelium forms an important part of the vasculature and is involved in promoting an atheroprotective environment via the complementary actions of endothelial cell-derived vasoactive factors. Disruption of vascular homeostasis can lead to the development of endothelial dysfunction which in turn contributes to the early and late stages of atherosclerosis. In recent years an increasing number of non-invasive vascular tests have been developed to assess vascular structure and function in different clinical populations. The present review aims to provide an insight into the anatomy of the vasculature as well as the underlying endothelial cell physiology. In addition, an in-depth overview of the current methods used to assess vascular function and structure is provided as well as their link to certain clinical populations.

No MeSH data available.


Related in: MedlinePlus

Endothelial nitric oxide production and it actions in the vascular smooth muscle cell. ACh= acetylcholine; BK= bradykinin; ATP= adenosine triphosphate; ADP= adenosine diphosphate; SP= substance P; SOCa2+= store-operated Ca2+ channel; ER= endoplasmic reticulum; NO= nitric oxide; sGC= soluble guanylyl cyclase; cGMP= cyclic guanosine-3’, 5-monophosphate; MLCK= myosin light chain kinase. *When Ca2+ stores of the endoplasmic reticulum are depleted a signal is sent to SOCa2+ channel which allows extracellular Ca2+ into the endothelial cell.
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Figure 1: Endothelial nitric oxide production and it actions in the vascular smooth muscle cell. ACh= acetylcholine; BK= bradykinin; ATP= adenosine triphosphate; ADP= adenosine diphosphate; SP= substance P; SOCa2+= store-operated Ca2+ channel; ER= endoplasmic reticulum; NO= nitric oxide; sGC= soluble guanylyl cyclase; cGMP= cyclic guanosine-3’, 5-monophosphate; MLCK= myosin light chain kinase. *When Ca2+ stores of the endoplasmic reticulum are depleted a signal is sent to SOCa2+ channel which allows extracellular Ca2+ into the endothelial cell.

Mentions: Inactive eNOS is bound to the protein caveolin and is located in small invaginations in the cell membrane called caveolae [22]. When intracellular levels of Ca2+ increase, eNOS detaches from caveolin and is activated [22]. NO agonists can influence the detachment of eNOS from caveolin by releasing Ca2+ from the endoplasmic reticulum (Fig. 1) [23]. Examples of such NO agonists include bradykinin (BK), acetylcholine (ACh), adenosine tri-phosphate (ATP), adenosine di-phosphate (ADP), substance P and thrombin [24]. Once intracellular Ca2+ stores are depleted a signal (thus far unidentified) is sent to the membrane receptors to open Ca2+ channels allowing extracellular Ca2+ into the cell [25, 26]. This process of Ca2+ regulation is known as store-operated Ca2+ entry or capacitative Ca2+ entry [27]. Ca2+ attaches to the protein calmodulin in the cytoplasm of the cell, after which it undergoes structural changes which allows it to bind to eNOS [28]. eNOS then converts L-arginine into NO [16]. This pathway of NO production is represented in Fig. (1) below. It is important to highlight that this mechanism of NO production is dependent on the levels of intracellular Ca2+ in the endoplasmic reticulum as well as Ca2+ which diffuses into the cell from extracellular stores. A reduction in Ca2+ causes the calcium-calmodulin complex to dissociate from eNOS, which in turn binds with caveolin and becomes inactivated [28].


The endothelium and its role in regulating vascular tone.

Sandoo A, van Zanten JJ, Metsios GS, Carroll D, Kitas GD - Open Cardiovasc Med J (2010)

Endothelial nitric oxide production and it actions in the vascular smooth muscle cell. ACh= acetylcholine; BK= bradykinin; ATP= adenosine triphosphate; ADP= adenosine diphosphate; SP= substance P; SOCa2+= store-operated Ca2+ channel; ER= endoplasmic reticulum; NO= nitric oxide; sGC= soluble guanylyl cyclase; cGMP= cyclic guanosine-3’, 5-monophosphate; MLCK= myosin light chain kinase. *When Ca2+ stores of the endoplasmic reticulum are depleted a signal is sent to SOCa2+ channel which allows extracellular Ca2+ into the endothelial cell.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3040999&req=5

Figure 1: Endothelial nitric oxide production and it actions in the vascular smooth muscle cell. ACh= acetylcholine; BK= bradykinin; ATP= adenosine triphosphate; ADP= adenosine diphosphate; SP= substance P; SOCa2+= store-operated Ca2+ channel; ER= endoplasmic reticulum; NO= nitric oxide; sGC= soluble guanylyl cyclase; cGMP= cyclic guanosine-3’, 5-monophosphate; MLCK= myosin light chain kinase. *When Ca2+ stores of the endoplasmic reticulum are depleted a signal is sent to SOCa2+ channel which allows extracellular Ca2+ into the endothelial cell.
Mentions: Inactive eNOS is bound to the protein caveolin and is located in small invaginations in the cell membrane called caveolae [22]. When intracellular levels of Ca2+ increase, eNOS detaches from caveolin and is activated [22]. NO agonists can influence the detachment of eNOS from caveolin by releasing Ca2+ from the endoplasmic reticulum (Fig. 1) [23]. Examples of such NO agonists include bradykinin (BK), acetylcholine (ACh), adenosine tri-phosphate (ATP), adenosine di-phosphate (ADP), substance P and thrombin [24]. Once intracellular Ca2+ stores are depleted a signal (thus far unidentified) is sent to the membrane receptors to open Ca2+ channels allowing extracellular Ca2+ into the cell [25, 26]. This process of Ca2+ regulation is known as store-operated Ca2+ entry or capacitative Ca2+ entry [27]. Ca2+ attaches to the protein calmodulin in the cytoplasm of the cell, after which it undergoes structural changes which allows it to bind to eNOS [28]. eNOS then converts L-arginine into NO [16]. This pathway of NO production is represented in Fig. (1) below. It is important to highlight that this mechanism of NO production is dependent on the levels of intracellular Ca2+ in the endoplasmic reticulum as well as Ca2+ which diffuses into the cell from extracellular stores. A reduction in Ca2+ causes the calcium-calmodulin complex to dissociate from eNOS, which in turn binds with caveolin and becomes inactivated [28].

Bottom Line: The endothelium forms an important part of the vasculature and is involved in promoting an atheroprotective environment via the complementary actions of endothelial cell-derived vasoactive factors.The present review aims to provide an insight into the anatomy of the vasculature as well as the underlying endothelial cell physiology.In addition, an in-depth overview of the current methods used to assess vascular function and structure is provided as well as their link to certain clinical populations.

View Article: PubMed Central - PubMed

Affiliation: School of Sport and Exercise Sciences, University of Birmingham, Birmingham, West Midlands, United Kingdom.

ABSTRACT
The endothelium forms an important part of the vasculature and is involved in promoting an atheroprotective environment via the complementary actions of endothelial cell-derived vasoactive factors. Disruption of vascular homeostasis can lead to the development of endothelial dysfunction which in turn contributes to the early and late stages of atherosclerosis. In recent years an increasing number of non-invasive vascular tests have been developed to assess vascular structure and function in different clinical populations. The present review aims to provide an insight into the anatomy of the vasculature as well as the underlying endothelial cell physiology. In addition, an in-depth overview of the current methods used to assess vascular function and structure is provided as well as their link to certain clinical populations.

No MeSH data available.


Related in: MedlinePlus