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Type-1
angiotensin II
receptor
Type-1
angiotensin II
receptor
Type-1
angiotensin II
receptor
NMDA Receptor
Excitatory
amino acid
transporter 3
Cathepsin G
Chymase
Angiotensinogen
Renin
Angiotensin II
L-Glutamic acid
Vasopressin
Aldosterone
L-Glutamic acid
Na
+
H
+
H
+
Angiotensin I
Angiotensin-
converting
enzyme
Azilsartan medoxomil
Vasopressin
Release
Vasocontriction
Thirst
Sensation
Aldosterone
Production
Type-1
angiotensin II
receptor
Zinc (II) ion
Chloride ion
Na
+
Aldosterone is associated
with salt and water
retention in the kidneys
raising blood pressure but
less activation from
angiotensin II leads to less
water and salt retention
keeping blood pressure from
rising.
Basal Membrane
Blood Vessel
Angiotensin II can act on
angiotensin II type 1
receptors (AT1) in the
tunica media of the smooth
muscles lining blood vessels
causing vasoconstriction
which increases blood
pressure. Inhibition of
angiotensin II creation
lowers the blood pressure as
vasoconstriction does not
occur.
Angiotensin from the liver
that circulates in the blood
is converted to angiotensin
I and angiotensin II through
renin and the angiotensin
converting enzyme
respectively that are from
the kidneys and lungs.
Azilsartan medoxomil
inhibits the Type 1
angiotensin II receptor
therefore blocking the
action of angiotensin II.
This decreases the effect of
circulating angiotensin II
impacting various areas of
the body which regulate
blood pressure.
Angiotensin II type 1
receptors (AT1) on the basal
membrane of the kidneys are
activated by angiotensin II
to increase aldosterone
production. Lower levels of
angiotensin II due to
benazepril inhibition
decrease aldosterone
production.
Posterior Pituitary Gland
AT1 receptors in the
posterior pituitary gland
cause the release of
vasopressin after activation
of angiotensin II.
Vasopressin
Vasopressin is a
anti-diuretic hormone that
causes water reabsorption in
the kidneys increases blood
pressure. Vasopressin also
causes smooth muscle
contraction in blood vessels
also increasing blood
pressure. Benazepril
inhibits the amount of
vasopressin being released
due to AT1 activation
keeping blood pressure form
rising.
Hypothalamus
Paraventricular Nucleus
Neuron (PVN Neuron)
Astrocyte
Angiotensin II activates AT1
receptors on astrocyte in
the hypothalamus. The AT1
receptor is responsible for
the inhibition of the
excitatory amino acid
transporter 3 which uptakes
glutamate.
Due to less angiotensin II
production, there is less
inhibition of the glutamate
transporter which leads to
more uptake of glutamate to
astrocytes. Less glutamate
is avaliable to bind to NMDA
receptors on paraventricular
nucleus neurons (PVN
neurons). PVN neurons are
responsible for thirst
sensation. Less glutamate
stimulus decreases thirst
sensation.
Kidney Cell
Melanosome
AGTR1
AGTR1
AGTR1
GRIN2A
SLC1A1
CTSG
CMA1
AGT
REN
Angiotensin II
L-Glutamic acid
Vasopressin
Aldosterone
L-Glutamic acid
Sodium
Hydrogen Ion
Hydrogen Ion
Angiotensin I
ACE
Azilsartan
medoxomil
Vasopressin
Release
Vasocontriction
Thirst
Sensation
Aldosterone
Production
AGTR1
Sodium