Status
Please wait ...
EndoNet
The information resource about the endocrine network in human.
Search
Search a component
Browse
Browse pathways
Browse hormones
Browse hormones functions
Browse hormone classification
Browse receptors
Network
Load network
Path analysis
Process network
Help
Help
Statistic
About
Details for phenotype: hypertension
Top
General information
Triggers
Toolbox
Click to access the toolbox
Top
General information
Triggers
Toolbox
Click to access the toolbox
EndoNet ID: ENP00475
Add to network
Name
hypertension
General information
This phenotype is pathologic
Glucocorticoid-induced elevation in blood pressure is well documented in humans.
[1]
Links to other resources
GO
regulation of blood pressure
OMIM
145500
Medline Plus
000468
MeSH term
D006973
Disease database
6330
Phenotype triggers
more activity (high ligand concentration, overexpression) of
glucocorticoid receptor
ui-button
in
macrophage
ui-button
Oxidative stress and nitric oxide deficiency are emerging as key components in the pathogenesis of glucocorticoid-induced hypertension.
[2]
This highlights the role of inflammation and oxidative stress in the pathogenesis of glucocorticoid-induced hypertension and this is consistent with a role for macrophages in this pathology.
[3]
more activity (high ligand concentration, overexpression) of
mineralcorticoid receptor
ui-button
in
macrophage
ui-button
Activation of an MR, in the context of inappropriate sodium status, has major cardiovascular pathophysiological consequences including hypertension.
[3]
Chronic inappropriate activation of an MR is well recognised to promote hypertension. Excess plasma mineralocorticoids promote sodium and water retention and potassium secretion leading to the maintenance of blood pressure at a higher set point.
[4]
MR antagonists have been shown to be effective anti-hypertensive agents in essential hypertension, suggesting a role for MR signalling in hypertension.
[5]
Reference