ENDOTHELIAL DYSFUNCTION IN HYPERTENSION - conversion by arginase by the lack of action of eNOS
RISK FOR AVE generates accumulation of antioxide anion → is a reactive
species of oxygen → oxidative stress!
It generates the formation of other types of reactive oxygen
species, such as hydrogen peroxide and peroxinitrito →
block the potassium channel that nitric oxide seeks to open →
prevent cell relaxation.
Phospholipase and A2 accumulation of → formation of more
atheadonic acid and more COX 1 and COX 2 = inflammatory
substances.
Formation of thromboxane and plostaglandina → causes
opening of the calcium channel → enters and does contraction.
Most actions of NO are mediated via the production of cGMP by
guanylate cyclase, resulting in a decreased intracellular calcium
(Ca2+) concentration. Lower intracellular Ca2+ results in
Hypertension → hemodynamic stress and → endothelial
relaxation of the vascular smooth muscle layer and ultimately in
dysfunction → vasoconstriction → increases endurance.
vasodilatation and a decrease in blood pressure.
Constriction and relaxation factors derived from the endothelium
In very hypertensive patients, it may have increased pulsation
itself. There is a balance between the release of these
substances. pressure. This increase reaches the capillaries and generates
mini-pulses that gwas injury and endothelial dysfunction
causing increased permeability due to loss of occlusive
MICROVASCULATURE
function.
External ethyl of the parasympathetic → releases acetylcholine
for example → internally, in the endothelial cell, has a stimulus for When you have hypertension, sometimes endothelial dysfunction
nitric oxide synthase to begin to actand stimulates the is so great that it has prejudício in the communicating junctions
conversion between oxygen and arginine into nitric oxide → increases permeability facilitating the passage of toxic
substances in the CNS (such as urea) → harms neurons and
and citrulline.
astrocytes.
Astrocytes sustain neurons and → greatly facilitates the risk of
microhemorrhages. In the long run, these microhemorrhages
have decreased neuron function and synapses → decline of
central → long-term cognitive decline.
Joining with elderly patients and cognitive decline of age,
these microhemorrhages increase the risk of dementia.
The nitric oxide produced and released by the endothelial cell has
paracrina action on the smooth muscle cell → acts on guanilil
cilcase facilitating the relaxation of smooth múscularcells.
Hypertensive/chronic hyperglycemia/smoker has higher
hemodynamic stress → the blood forces more against the vessel
wall. These conditions cause the vasodilator stimulus to act on
the specific receptor, but due to the condition, the nitric oxide
syntha enzyme is not coupled → when calcium increases in
the endothelial cell, phosphoylate compounds of tyrosine
instead of serine! It doesn't make the enzyme work properly!
ENOS problems do not work:
1. It uses less oxygento form nitric oxide → little nitric oxide will
be formed → lower stimulation for vasodilation.
2. As the enzyme does not work right and tyrosine phosphoryl
rather than serine → does not use arginine → has more
arginase → turns arginine into ornithine and urea. This
RISK FOR AVE generates accumulation of antioxide anion → is a reactive
species of oxygen → oxidative stress!
It generates the formation of other types of reactive oxygen
species, such as hydrogen peroxide and peroxinitrito →
block the potassium channel that nitric oxide seeks to open →
prevent cell relaxation.
Phospholipase and A2 accumulation of → formation of more
atheadonic acid and more COX 1 and COX 2 = inflammatory
substances.
Formation of thromboxane and plostaglandina → causes
opening of the calcium channel → enters and does contraction.
Most actions of NO are mediated via the production of cGMP by
guanylate cyclase, resulting in a decreased intracellular calcium
(Ca2+) concentration. Lower intracellular Ca2+ results in
Hypertension → hemodynamic stress and → endothelial
relaxation of the vascular smooth muscle layer and ultimately in
dysfunction → vasoconstriction → increases endurance.
vasodilatation and a decrease in blood pressure.
Constriction and relaxation factors derived from the endothelium
In very hypertensive patients, it may have increased pulsation
itself. There is a balance between the release of these
substances. pressure. This increase reaches the capillaries and generates
mini-pulses that gwas injury and endothelial dysfunction
causing increased permeability due to loss of occlusive
MICROVASCULATURE
function.
External ethyl of the parasympathetic → releases acetylcholine
for example → internally, in the endothelial cell, has a stimulus for When you have hypertension, sometimes endothelial dysfunction
nitric oxide synthase to begin to actand stimulates the is so great that it has prejudício in the communicating junctions
conversion between oxygen and arginine into nitric oxide → increases permeability facilitating the passage of toxic
substances in the CNS (such as urea) → harms neurons and
and citrulline.
astrocytes.
Astrocytes sustain neurons and → greatly facilitates the risk of
microhemorrhages. In the long run, these microhemorrhages
have decreased neuron function and synapses → decline of
central → long-term cognitive decline.
Joining with elderly patients and cognitive decline of age,
these microhemorrhages increase the risk of dementia.
The nitric oxide produced and released by the endothelial cell has
paracrina action on the smooth muscle cell → acts on guanilil
cilcase facilitating the relaxation of smooth múscularcells.
Hypertensive/chronic hyperglycemia/smoker has higher
hemodynamic stress → the blood forces more against the vessel
wall. These conditions cause the vasodilator stimulus to act on
the specific receptor, but due to the condition, the nitric oxide
syntha enzyme is not coupled → when calcium increases in
the endothelial cell, phosphoylate compounds of tyrosine
instead of serine! It doesn't make the enzyme work properly!
ENOS problems do not work:
1. It uses less oxygento form nitric oxide → little nitric oxide will
be formed → lower stimulation for vasodilation.
2. As the enzyme does not work right and tyrosine phosphoryl
rather than serine → does not use arginine → has more
arginase → turns arginine into ornithine and urea. This
