Cardiac Drugs.
Part 1 of 5
Starting a new series on some of those cardiac drugs that we all give and probably take for granted.
Let's start with some physiology of hypertension. We all know that blood vessels stiffen and become hardened (sclerosis) with age. With a reduction in flow, arteries in kidneys detect low flow, and stimulate the release of a protein called Renin from the juxtoglomerular cells.
Renin converts a protein in plasma to Angotensin.
Angiotensin in plasma is converted to an active state by Angiotensin Converting Enzyme (ACE) secreted in the lungs.
This conversion by ACE to angiotensin 2 causes potent chemical constriction of blood vessels , and elevates BP.
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In patients with Heart Failure , high blood pressure makes the heart have to work so much harder to pump blood, that it actually fails, and heart failure worsens.
Less blood being pumped = Lower output = Lower kidney flow = More Renin!!! It is a viscous cycle.
So a class of drug that impairs this situation is an ACE inhibitor.
***pril
These drugs all have the suffix 'pril in their generic name.
Lisinopril
Perindopril
Ramipril
Captopril
Enalpril
All examples of these ACE inhibitor drugs. By stoping ACE , these drugs inhibit the conversion of Angiotensin 1 into the active Angiotensin 2 which causes high blood pressure.
These drugs are not without their side effects. In fact, the side effects like annoying dry cough are often the reason for non compliance with this therapy.
An Increase of inflammatory pain caused by the release of Bradykinin when ACE is inhibited can make these drugs literally a Pain to take. This problem usually results in a need to switch therapy to the Sartan drugs.
And that is our next article.
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