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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 Neprilysin Cathepsin G Chymase Angiotensinogen Renin Angiotensin II L-Glutamic acid Candoxatrilat Vasopressin Aldosterone L-Glutamic acid Na+ H+ H+ Candoxatrilat Angiotensin I Candoxatril Angiotensin- converting enzyme Vasopressin Release Vasocontriction Thirst Sensation Aldosterone Production Type-1 angiotensin II receptor 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 After ingestion of Candoxatril, it is converted to Candoxatrilat in the liver and returned to circulate back into the blood. Hepatocyte 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. Candoxatrilat inhibits the enzyme angiotensin converting enzyme (ACE) therefore blocking the conversion of angiotensin I into angiotensin II. This decreases the amount of circulating angiotensin II levels 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 Candoxatrilat 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. Candoxatrilat 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 Neprilysin acts to degrade Angiotensin II and natriuretic peptides. With Neprilysin inhibited it allows natriuretic peptides to act to increase vasodilation, natriuresis and decreasing blood pressure.
AGTR1 AGTR1 AGTR1 GRIN2A SLC1A1 MME CTSG CMA1 AGT REN Angiotensin II L-Glutamic acid Candoxatrilat Vasopressin Aldosterone L-Glutamic acid Sodium Hydrogen Ion Hydrogen Ion Candoxatrilat Angiotensin I Candoxatril ACE Vasopressin Release Vasocontriction Thirst Sensation Aldosterone Production AGTR1 Sodium
AGTR1 AGTR1 AGTR1 GRIN2A SLC1A1 MME CTSG CMA1 AGT REN Ang II Glu Cando ADH Aldostr Glu Na+ H+ H+ Cando Angio1 Candoxa ACE Vas Rel Vasoc Thi Sen Ald Pro AGTR1 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 After ingestion of Candoxatril, it is converted to Candoxatrilat in the liver and returned to circulate back into the blood. Hepatocyte 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. Candoxatrilat inhibits the enzyme angiotensin converting enzyme (ACE) therefore blocking the conversion of angiotensin I into angiotensin II. This decreases the amount of circulating angiotensin II levels 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 Candoxatrilat 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. Candoxatrilat 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 Neprilysin acts to degrade Angiotensin II and natriuretic peptides. With Neprilysin inhibited it allows natriuretic peptides to act to increase vasodilation, natriuresis and decreasing blood pressure.
AGTR1 AGTR1 AGTR1 GRIN2A SLC1A1 MME CTSG CMA1 AGT REN Ang II Glu Cando ADH Aldostr Glu Na+ H+ H+ Cando Angio1 Candoxa ACE Vas Rel Vasoc Thi Sen Ald Pro AGTR1 Na+