JOHANÉ DE LA REY
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JOHANÉ DE LA REY

Blog #2.2

14 Nov 2021, 16:12 Publicly Viewable
  • Hypertension increases angiotesinogen levels. Angiotensinogen is converted to Angiotensin I by Renin. Angiotensin I is converted to Angiotensin II which binds to the receptors and causes the release of aldosterone and ADH. Aldosterone stimulates the increased reabsorption of Na+ and H2O and increased excretion of K+. ADH stimulates the increased reabsorption of H2O. Both leads to an increase in blood pressure. 
  • ACE inhibitors in addition to converting ANGI to ANG II, also inhibit the degradation of bradykinin, substance P, and interleukins. The inhibition of bradykinin metabolism leads to increased bradykinin levels which causes side effects, like cough and angioedema. With the inhibition of angiotensin receptors these side effects are not present.
  • ACE inhibitors block the conversion of ANG I to ANG II. ACE inhibitors also inhibit the metabolism of bradykinin to inactive peptides. This contributes to the decrease in blood pressure and treats hypertension.
  • Losartan and similar drugs act on the angiotensin AT1 receptors. They have an indirect effect on the ANG II receptors. When these drugs are given for a long period of time they disinhibit renin release and increase the ANG II levels that circulate in the body. That increases the stimulation of AT2 receptors.
  • Kinins causes vasodilation in arteries and vasoconstriction in veins. Autacoids play a role, because during vasodilation the release of nitric oxide or vasodilator prostaglandins for example PGE2 and PGI2 is mediated. During vasoconstriction there is a release of vasoconstrictor prostaglandins such as PGF2α.
  • The B2 receptor.
  • ANP causes urine flow and sodium excretion. The natriuresis induced by the ANP is because of an increase in glomerular filtration rate and decreased proximal sodium reabsorption. ANP inhibits the release of renin, aldosterone and AVP, which causes increased sodium and water excretion. ANP also causes vasodilation and all these effects contribute to the treatment of hypertension and congestive heart failure.
  • Neprilysin is responsible for the degeneration of natriuretic peptides in the lungs, kidneys and liver. It is also a neutral endopeptidase. Neprilysin inhibition causes ANP and BNP levels to increase in the circulation, causing diuresis and natriuresis. It increases protective natriuretic peptides. The inhibitor's name is Sacubitril.
  • Bosentan, macitentan, ambrisentan and sitaxsentan.