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To understand what an Angiotensin receptor blocker medication does, it is helpful to know the renin-angiotensin-aldosterone system (RAAS).
Renin is a hormone that is released from the Juxtaglomerular (JG) cells that are located in the kidneys. The JG cells are stimulated to release renin when the blood pressure is low.
The liver also senses low blood pressure and sends out its own messenger/hormone called angiotensinogen.
When renin meets up with angiotensinogen, it thinks that angiotensinogen is too long of a word as well as too long of a protein and cuts off part of the protein turning it into angiotensin I. Angiotensin I floats through the bloodstream until it meets up with the endothelial cells which have angiotensin converting enzymes (ACE) on them. ACE converts Angiotensin I to Angiotensin II. Oh hey, by the way, guess where an ACE inhibitor is going to be working? Right here, stopping the ACE inhibitor from converting Angiotensin I to II.
Angiotensin II does a couple of things that all lead to increased blood pressure. An easy way to remember this is by replacing angiotensin with angio (blood vessel) -tensin think of tension. Like the blood vessel is tense or the tension is increased in the blood vessel and this makes higher blood pressure. So how does it do this?
- First it constricts the smooth muscle cells in blood vessels (vasoconstriction)
- Second it tells the kidneys to produce less urine by holding onto the salt. And guess what follows salt?: Water
- Third it tells the pituitary gland to secrete antidiuretic hormone (ADH) which tells the kidneys to hold onto water
- Fourth it stimulates the adrenal glands to secrete aldosterone which goes to the kidney and tells the kidney to hold onto salt, which as we said before, holds onto water
What is an Angiotensin II receptor blocker (ARB)?
So the ARB medications will block angiotensin II from binding to their receptors. Last week we covered ACE inhibitors, and like I talked about above, those stop the creation of Angiotensin II. However, with Angiotensin II receptor blockers, the Angiotensin II is created but the receptor has a little ninja swatting away the angiotensin II saying, “Not today my friend.”
So if you deny the body something that makes the blood pressure increase, naturally you will be lowering blood pressure. Yay for opposites!
What is an angiotensin receptor?
These little buggers are located in cell walls of the smooth muscles. Our arteries have smooth muscles and when the receptors are stimulated they contract. Naturally, blocking the cell from contracting will relax the smooth muscles, decreasing blood pressure.
What are the ARB drugs used for?
Well, I’m sure you could have guessed that the most common thing that ARBs are used for is to lower blood pressure. But it can also help treat kidney failure.
Remember RAAS (from the beginning of this post?) Well Angiotensin II will affect the blood pressure via the kidneys so if we give an ARB, the kidneys are stimulated to lose the salt and water. This flushing of the kidneys takes the other waste products with it… like say creatinine or urea nitrogen (BUN).
Here is a list of Angiotensin II Receptor Blockers:
- valsartan (Diovan)
- losartan (Cozaar)
- Phenobarbital is contraindicated with losartan because the metabolism of these medications fight for attention making both medications less effective.
- olmesartan (Benicar)
- azilsartan (Edarbi)
- candesartan (Atacand)
- eprosartan (Teveten)
- irbesartan (Avapro)
- telmisartan (Micardis)
Notice they all end in -sartan? At the very least, it is easy remember the Angiotensin II Receptor Blocker medication names!
In my practice, I administer losartan and valsartan most often. I also see patients prescribed losartan and valsartan the most. If I were trying to study these medications for my practice I would remember that -sartans are the ARBS, and then focus on losartan and valsartan specifics. That way, you know these off the top of your head, and if you see another -sartan you know it’s an ARB and then you can look it up easier.
I also see a combination therapy of hydrochlorothiazide with the ARB. These medications are as follows:
- Hydrochlorothiazide with losartan
- Diovan HCT
- Hydrochlorothiazide with valsartan
What are the side effects of angiotensin receptor blockers?
Nurses!! Take note: this medication type has the side effect of angioedema… AKA swelling to the throat, tongue, lips, basically the whole head so we are worried about airway with these patients! If the patient starts to get hoarseness, think airway and grab emergency airway equipment just in case.
Scary side effects aside, patients can develop a dry cough. Which is super annoying, like stub your toe level of inconvenience mixed with enough pain to suck but not enough to be debilitating.
Wait… doesn’t this sound a lot like ACE inhibitors? Yup. ACE inhibitors and ARBs both work on the Renin-Angiotensin-Aldosterone System and have the same side effects… but they are less likely to happen with ARBs. So a pro to ARBs is less chance of side effects.
I don’t know about you, but anytime I can group side effects of medications together like ACE inhibitors and ARBs I get warm fuzzies and celebrate the fact that I will have more room in my brain to remember things like memes and song lyrics.
ARBs vs ACE inhibitors
So the natural question to ask then is if these medications are so similar, why would I give one versus the other?
ACE inhibitors are the preferred and first line antihypertensive medication because studies show that when compared, patients who took ACE inhibitors were less likely to have outcomes involving stroke or heart attack. Ace inhibitors also have cardioprotective qualities, especially in patients with diabetes. Let’s be real, in the united states, we take care of diabetics as frequently as we drink coffee, so like, every day.
However, ACE inhibitors also are more likely to have side effects than an ARB. So If a patient has an allergic reaction or adverse effects, an ARB will be considered. ARBs do not have the dry cough side effect as much as an ACE inhibitor does and ARBs have a smaller chance of angioedema.
ACE inhibitors vs ARBs is not so clear-cut because there are risks involved with both, but if a patient can tolerate an ACE inhibitor then it is the best outcome for them. If they are not able to tolerate an ACE inhibitor then an ARB is a good second line choice.
- Make sure your patients know not take ARBs with salt substitutes containing potassium. If they are on a low sodium diet, make sure they follow the diet EXACTLY as the doctor prescribes it.
- ARBs are less effective in African Americans.
- Nurses, please, take a blood pressure and a heart rate before you give this medication and obviously do not give the ARB if your patient has a low heart rate or a low blood pressure.
- Warn patients to change their positions slowly to avoid a syncopal episode due to an orthostatic hypotension event.
- Please ask your patients when they normally take their ARBs and try to administer them at the same time that they normally take this medication.
- If your patient stops taking this medication suddenly expect a reflex hypertension to occur.
- Do not give ARBs to anyone who is pregnant. It can cause injury or death to a developing fetus.
- American Family Physician
- National Institute of Health
- American Diabetes Association
- American Heart Association
- Pharmacology: A Nursing Process Approach
Written by: ME!! Susan DuPont BSN, RN, CEN of bossrn.com who is a staff nurse at a level I trauma emergency department. She loves dogs, hunting, fishing, being outside and practicing/enhancing her survival skills.
Check out our other Matters of the Heart post in our series!
- Normal Sinus Rhythm
- Cardiac Arrest
- Heart Attack
- Premature Atrial Contractions (PACs)
- Junctional Rhythms
- Supraventricular Tachycardia (SVT)
- Atrial Fibrillation & Atrial Flutter
- Premature Ventricular Contractions (PVCs)
- Ventricular Tachycardia (Vtach)
- Ventricular Fibrillation (Vfib)
- Torsades de Pointes (TdP)
- Beta Blockers
- Calcium Channel Blockers
- ACE Inhibitors
- Angiotensin II Receptor Blockers (ARBs)
- Deep Vein Thrombosis (DVT)
- Pulmonary Embolisms (PE)
- Peripheral Vascular Disease (PVD)
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