• Justin Crespo- Guest Blogger

ACE’s and ARB’s (bro-science)


The Science of ACE’s and ARB’s

To really know how Angiotensin Converting Enzyme (ACE Inhibitors) and Angiotensin Receptor Blockers (ARB) work, we must understand some physiology. Like my favorite teacher, Mrs. Frizzle, from ‘Magic School Bus’, always use to say, “Let’s get messy, take chances, and make mistakes!”

What the heck is RAAS??

Renin-Angiotensin-Aldosterone-System (RAAS) is the key behind understanding how ACE’s and ARB’s work. It is a system of enzymatic reactions that cause an increase in blood pressure from low blood pressure triggers or certain nerves under stress (catecholamines like epinephrine). The body’s way of saying “Yo! I need more blood to the core!”

Think of it like this, when your body needs to increase blood pressure to either supply more blood to vital organs, or as a reaction from vasodilation (hypotension), the RAAS system increases blood pressure by creating peripheral vasoconstriction and then BAM! homeostatic condition is met. Normal blood pressure. However, like all things that sound wonderful, there is a downside. RAAS system can be activated more often than normal by stress. Yeah! The same kind of stress from work! That’s why stress can negatively affect your body. Moral of the story, drink wine. Kidding!

Let’s dive deeper.

Renin (the first word of RAAS) is an enzyme that in produced by the kidney’s that promotes the production of Angiotensin (AT). The process is relatively simple to comprehend. AT converts into AT-1 with the help of renin. AT-1 converts to AT-2 by the Angiotensin Converting Enzyme (ACE). Starting to sound familiar? Further breaking down, AT-2 connects to AT-1 receptor and AT-2 receptor. Then, AT-1 receptor activates Aldosterone, hence why it’s called Renin-Angiotensin-Aldosterone-System. The result is increased blood pressure. Aldosterone causes the kidneys to hold onto more sodium, which leads to more water staying in the body. The more fluid the body holds onto, the higher the blood pressure may become. To make it easier to understand, here’s a diagram.

ACE’s and ARB’s

Now that we understand RAAS, we’ll know how ACE’s and ARB’s work. The ACE inhibitors prevent the AT-1 to convert into AT-2, hence why it’s called ACE inhibitor.

The other factor that it works on is Bradykinin. What the heck is that?? AT-1 assists in the metabolism of Bradykinin. Picture this, AT-1 says to Bradykinin, “Hey man, I’ll help you grow” and then bradykinin can grow because of AT-1. To keep it simple, it is part of the inflammation process and it helps with lowering blood pressure.

Allow me to explain. When tissue is injured, the endothelial cells release bradykinin into the blood and help start the inflammation process (it helps protect the injured area). Bradykinin then releases several chemicals including Nitric Oxide.

You’re probably wondering, “Why do I have to know this??”

I promise it’s important! Well, Nitric Oxide (NO) is a potent vasodilator (lowers the blood pressure). If you’re thinking that’s how Nitroglycerin works, you’re right!! It’s a NO agonist, it releases NO into the blood to lower the pressure! ACE inhibitors prevent Bradykinin transforming into other peptides, therefore increasing the amount of bradykinin and BAM lowers blood pressure. You see how things are coming together?!

ARB’s (Angiotensin Receptor Blocker) is even easier to understand. To recall to the diagram, AT-2 connect to two receptors, you guessed it! AT-1 receptor and AT-2 receptor. AT-1 receptor then activates into aldosterone. So, if we say “No way, dude. You’re not connecting your AT-2 to my AT-1 receptor!” Aldosterone cannot be made, and BOOM! Your blood pressure doesn’t increase. Life saved..... well kinda.

The science of ACE’s and ARB’s rely heavily on the Renin-Angiotensin-Aldosterone-System which is responsible for increasing blood pressure. ACE Inhibitors prevent the transformation from AT-1 to AT-2 and prevents the transformation of bradykinin to other peptides which increases the amount of bradykinin. AT-1 helps metabolize bradykinin which then helps start the process of inflammation and releases NO into the blood resulting in lowering blood pressure. ARB’s block the receptor from AT-2 to attaching to it, preventing the creation of aldosterone. I hope this article helps you understand the entire process, the science of RAAS and ACE’s and ARB’s.

Justin Crespo, Flight Paramedic