Category Archives: ACE Inhibitors and ARBs

ACE Inhibitors: The No-Thrill -Prils

Never heard of angiotensin converting enzyme (ACE)?  Check out the post on the Renin-Angiotensin-Aldosterone System (RAAS) for a quick rundown.

ACE Inhibitors (prototype: captopril (Capoten)) are actually very thrilling.  However, the title of this little piece is referring to the other kind of thrill (scratch that, there are too many and some are quite disturbing), vascular thrills, which are palpable vibrations felt over arteries.  You get these when there is turbulent blood flow. Lots of things can cause this, but one of the more common is a sclerotic plaque. Chronic high blood pressure, among other things, increases your risk for developing these buildups, which can lead to arterial blockage and heart attacks.  Avoid the thrills, take the -prils!  Some drug company really needs to hire me for advertising.

As you may have already guessed, ACE Inhibitors like captopril stop the action of ACE (duh). This inhibits the formation of angiotensin II, the protein that responds to a decreased glomerular filtration rate(in the kidneys) and in turn signals the brain and kidneys to release aldosterone (among other things) and constrict the blood vessels. In other words, if the kidneys aren’t sensing the right amount of blood flow coming into them, renin and aldosterone will be released to boost up blood pressure via vascular constriction.   The RAAS is a homeostatic mechanism–it keeps your blood pressure balanced–so this process of constriction and relaxation in the blood vessels is a normal occurence.  But what if your blood pressure is running high?  Inhibiting part of the RAAS will reduce the vasoconstriction, limiting further pressure damage to the vessel walls.  Right on!

I recently attended a lecture on antihypertensives (blood pressure medication) that was led by three (yes, three) pharmacists.  According to them,  ACE inhibitors are the #1 choice for high blood pressure in most patients. Of course, since no drug is entirely safe or selective, there are some patients for which ACE inhibitors are not the best choice.  Other commonly-used drug classes, like beta blockers, are often used as well.

Here are some important highlights of the ACE inhibitors.

1.  Most of their generic names end in -pril.  Enalopril, captopril, lisinopril…you get the idea. Prils for thrills.  ‘Lil -pril pill.

2. Like any antihypertensive, a common adverse effect is hypotension, especially orthostatic hypotension, which is a sudden drop in blood pressure when you sit up or stand up.  As you can imagine, this can be dangerous, so don’t forget to assess BP and educate your patient (or yourself!) before you give a -pril!

3. There are at least two kind of weird things that can happen while taking an ACE-inhibitor:

1) A very small percentage of people have a life-threatening hypersensitivity reaction to ACEIs.  It manifests itself as angioedema, a very quick and scary swelling of the eyelids, mouth, and airways.  This can occur even after the drug has been taken for quite some time, and it is a major deal breaker.  No more ACEIs for you, ever again!  Here, have some [other appropriate drug].

2) Some people, and this is more common, develop a dry, hacking cough.  Turns out that angiotensin II, which actually resides in the lungs, has this other responsibility.  When activated, it regulates the release of bradykinin in the bronchioles.  So if it is inhibited, a lot of bradykinin starts building up and irritating the heck out of your airways. Since there are so many options around, this symptom is generally a good reason to switch to another class of drug.

WHY IS THIS POST SO LONG?