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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 Vasopressin Release Vasocontriction Thirst Sensation Aldosterone Production Type-1 angiotensin II receptor Valsartan 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 (Extracellular Space) 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. Valsartan 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
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 Vasopressin Release Vasocontriction Thirst Sensation Aldosterone Production AGTR1 Valsartan Sodium
AGTR1 AGTR1 AGTR1 GRIN2A SLC1A1 CTSG CMA1 AGT REN Ang II Glu ADH Aldostr Glu Na+ H+ H+ Angio1 ACE Vas Rel Vasoc Thi Sen Ald Pro AGTR1 Valsart Zinc Cl 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 (Extracellular Space) 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. Valsartan 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
AGTR1 AGTR1 AGTR1 GRIN2A SLC1A1 CTSG CMA1 AGT REN Ang II Glu ADH Aldostr Glu Na+ H+ H+ Angio1 ACE Vas Rel Vasoc Thi Sen Ald Pro AGTR1 Valsart Na+