Protein Synthesis

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Valsartan is an Angiotensin (II) receptor blocker; it is a non-peptide orally active AT1 receptor antagonist. AT1 receptors are present in our blood vessels and heart tissues; and they are coupled to Gq proteins and IP3 signal transduction pathways that stimulate vascular smooth muscle cells contraction. The renin- angiotensin aldosterone system the one that generates angiotensin II, a vasoconstrictive hormone it causes the blood vessels to constrict and it is produced by the kidney. This system is inappropriately activated in patients with heart failure, and results in raised blood pressure, oedema and also ventricular remodelling who causes the heart to get bigger because of the ANG (II) effect; apart from being a vasoconstrictor it also …show more content…
Valsartan block the formation of ANG (II) and inhibits its actions, it dilate arteries therefore reducing arterial pressure, improving perfusion and reducing cardiac afterload thereby decreases blood pressure and makes it easier for the heart to contract. It also causes natriuresis by inhibiting the secretion of aldosterone and by reducing the direct stimulatory effect of ANG (II) on reabsorption of sodium and bicarbonate ions in the proximal convoluted tubule. AT1 antagonist also down regulate the sympathetic adrenergic activity and reverse the ventricular remodelling. Angiotensin receptor blockers (ARBs) and angiotensin converting enzyme inhibitors (ACEi) are the only type of medications that attacks the underlining cause of heart failure. ARBs do not inhibit the breakdown of bradykinin only ACE inhibitors do this. ACE inhibitors stop the production of ANG (II) but also stop the breakdown of bradykinin, the building up of bradykinin causes dry …show more content…
ANP is mainly released from the cardiac atria in response to increased atrial pressure and intravascular fluid overload. BNP is released from the left ventricle as a result of increased mean systemic pressure. ANP and BNP mechanisms of action include vasodilation, natriuresis and diuresis. These mechanisms are activated when the peptide proteins bind to ligand-gated ion channels receptors, these are coupled to guanylyl cyclase; activation of this receptor increases intracellular cyclic guanosine monophosphate. Cyclic GMP relaxes smooth muscle tissues. Atriuretic peptides are released in response to excess plasma volume (odema) and increasing volume of blood in the left ventricle (hypertrophy), enlargement of the heart to compensate for the decreased cardiac output. A common symptom found in patients with heart failure. Atriuretic peptides cause direct vasodilation, which result in deceased ventricular preload and vascular resistance. They also increase glomerular filtration rate, resulting in natriuresis and diuresis, therefore reducing the amount of sodium and water in the body. They decrease the production of RENIN the enzyme that is responsible for the production of angiotensin (II) resulting in vasodilation. Neprylisin is present in
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