Cardiovascular Agents. Michael Perez. Cardiovascular Disease. These are various and have innumerable amounts of treatments and drugs used in treatment Focus on hypertension and angina (chest pain.). Hypertension and angina.
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Both of these can be caused by constriction of the blood vessels in the body, or simply by an increase in blood flow in a vessel that isn’t dilated completely. This of course causes hypertension directly (high blood pressure) and leads to chest pains if these vessels deliver blood to the heart.
This is not definitive, but is considered the most likely way NO works:
target protein for nitric oxide is guanylyl cyclase, enzyme that generates cyclic GMP from GTP by causing a conformational change in guanylyl cyclase by binding to the allosteric site on the enzyme.
Cyclic GMP causes cylic GMP dependent kinase to become activated, which phosphorylates myosin light-chain kinase, making it inactive. This renders it unable to interact with calcium ions that bind to calmodulin and prevents phosphorylation of myosin that interacts with actin to cause the contraction of smooth muscle.
These drugs have become the alternative as of late to nitro-vasodilators in treating hypertension and angina.
These act in much the same way, only they directly block calcium from being released by cells that later binds to calmodulin, preventing phosphorylation of myosin that interacts with actin to cause smooth muscle contraction.
A tetralol derivative has been developed from rougly 500 derivatives of verapamil. This drug showed selectivity between vascular and cardiac tissues during assay screening and some clinical studies using a guinea pig heart. Still in trials.