Antihypertensive Medication Chart: Drug List, Classes, and Examples
Antihypertensive medications made easy! Chart includes antihypertensive drug classes along with their drug names, list of medication examples, mechanism of action, and how they decrease high blood pressure to treat hypertension!
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Antihypertensive Medication Chart
Antihypertensive drugs are medications used to treat high blood pressure, also known as hypertension.
There are several different classes, or categories, of antihypertensives based on their mechanism of action for lowering blood pressure.
The more common drug classifications include ACE inhibitors, angiotensin II receptor blockers or ARBs, alpha blockers, beta blockers, calcium channel blockers, and diuretics.
(ACE = Angiotensin-Converting Enzyme)
(ARB = Angiotensin II Receptor Blocker)
This post will provide you with an overview of the main antihypertensive classes.
We will use the antihypertensive chart below to walk through the main classes, along with their drug names, list of example medications, mechanism of action, and primary effect on blood pressure.
You will also learn memory tricks to remember the main antihypertensive classes along with the drug names within each class.
Let’s get started!
Antihypertensive Medication Chart: Main Drug Classes
Antihypertensive Drug Classes
Let’s start by giving you a simple trick to remember the main antihypertensive classes.
Antihypertensive Medications: Drug Classes
ABCD = Main Antihypertensive Classes
As mentioned above, antihypertensives are medications that treat high blood pressure or hypertension.
There are several different classes of antihypertensives, and they can be remembered using the acronym “ABCD”.
A = Ace Inhibitors
A = ARBs
A = Alpha Blockers
“A” will stand for several different antihypertensive medications with the first one being angiotensin-converting enzyme inhibitors, also known as ACE inhibitors.
The second “A” stands for angiotensin II receptor blockers, also known as ARBs
The final “A” stands for alpha blockers.
B = Beta Blockers
“B” will help you remember beta blockers.
C = Calcium Channel Blockers
The “C” stands for calcium channel blockers.
D = Diuretics
Finally the “D” is to help you remember diuretics.
While there are other antihypertensives out there, these are the main ones and generally the more common ones.
For example, there are also central agonists and vasodilators that can be used to lower blood pressure.
You can use the “C” to remember Central agonists, and you can use the “D” to remember Dilators for vasodilators.
Antihypertensive Medications: “ABCD” method for remembering the main classes
Antihypertensive Drug Names
Now that we know the main antihypertensive classes, let’s learn an easy way to remember the drug names within each class.
Antihypertensive Medications: Drug Names
Suffixes = Antihypertensive Drug Names
The simple trick to remember the medications within each antihypertensive drug class is to use the suffix of their name.
ACE Inhibitors = “pril”
ACE inhibitors usually end in “pril”
ARBs = “sartan”
Angiotensin II receptor blockers typically have the suffix “sartan”
Alpha Blockers = “osin” (Selective Alpha-1)
Alpha blockers end in “osin”, and many of the alpha blockers specific to treating hypertension end in “zosin”.
It is important to note that the suffix “osin” or “zosin” mainly applies to selective alpha-1 blockers.
There are also non-selective alpha-1 and alpha-2 blockers, and they typically end in “mine”.
Nonselective alpha blockers include phentolamine and phenoxybenzamine, which are considered in the treatment of pheochromocytoma and cocaine-induced hypertension.
Since nonselective alpha blockers are used more for catecholamine-induced hypertension, we will focus on selective alpha-1 antagonists for purposes of this post.
The EZmed alpha antagonist post will go into more detail on both the selective and nonselective types of alpha blockers.
**In short, be aware that “osin” mainly applies to selective alpha-1 blockers.
Beta Blockers = “lol”
Beta blockers usually have the suffix “lol”
Calcium Channel Blockers = “dipine” (Dihydropyridines)
Many (but not all) calcium channel blockers end in “dipine”, particularly the dihydropyridines.
There are 2 main types of calcium channel blockers - dihydropyridines and non-dihydropyridines.
Dihydropyridines are used more for hypertension as they predominately target blood vessels, while nondihydropyridines (verapamil and diltiazem) are used more for tachydysrhythmias as they predominately target the heart.
Since dihydropyridines are used more for hypertension, we will focus on those in this post.
The EZmed calcium channel blocker post will go into more detail on both the dihydropyridines and non-dihydropyridines.
**In short, be aware that the suffix “dipine” mainly applies to dihydropyridine calcium channel blockers.
Diuretics = “ide”
Finally, many (but not all) of the diuretics use the suffix “ide”
**While using these suffixes is a great way to remember most of the drug names within each antihypertensive class, there are exceptions and this is not a hard-and-fast rule.
Antihypertensive Medications: Drug name suffixes
Example Medications
Now that we know the drug name suffixes of each class, let’s take a look at some example medications.
Antihypertensive Medications: Example Drugs
ACE Inhibitors
We know ACE inhibitors typically end in “pril”.
Common examples include lisinopril and enalapril.
ARBs
Angiotensin II receptor blockers use the suffix “sartan”.
Common examples include losartan and valsartan.
Alpha Blockers
Alpha blockers, particularly the selective alpha-1 blockers, end in “osin”.
Examples include doxazosin and terazosin.
Beta Blockers
Example beta blockers include metoprolol and labetalol.
You can see how they end in “lol”
Calcium Channel Blockers
The dihydropyridine calcium channel blockers typically end in “dipine”.
Examples include amlodipine and nicardipine.
Diuretics
Finally, many (but not all) diuretics end in “ide”.
Examples include furosemide and hydrochlorothiazide.
Antihypertensive Medications: Drug Name Suffix and Examples
Antihypertensive Mechanism of Action
As we continue to move through the chart, let’s take a look at the mechanism of action of each antihypertensive drug class.
This will help us better understand how each medication is used to lower blood pressure.
Antihypertensive Medications: Mechanism of Action
ACE Inhibitors
As the name suggests, ACE inhibitors inhibit angiotensin-converting enzyme, also known as ACE.
Angiotensin-converting enzyme is part of the renin-angiotensin-aldosterone system.
Specifically, ACE is involved in converting angiotensin I into angiotensin II, which is the active hormone used to increase blood pressure through several mechanisms.
First, angiotensin II binds to angiotensin II receptors located on blood vessels. This causes vasoconstriction and an increase in blood pressure.
Angiotensin II also increases sodium and water reabsorption in the kidneys, and augments the release of aldosterone from the adrenal cortex and antidiuretic hormone from the posterior pituitary gland.
Renin Angiotensin Aldosterone System: Increases blood pressure through vasoconstriction, sodium/water reabsorption, aldosterone release, and antidiuretic hormone (ADH) release.
If we block angiotensin-converting enzyme with an ACE inhibitor, then we will decrease the conversion of angiotensin I to angiotensin II.
With lower levels of angiotensin II, we will not have the downstream effects of raising blood pressure.
ACE inhibitors are commonly used to treat hypertension (high blood pressure) as a result.
For more information about the mechanism of action, indications, side effects, and contraindications of ACE inhibitors, check out the ACE Inhibitor lecture.
ACE Inhibitor Mechanism of Action: Inhibits angiotensin-converting enzyme (ACE) from forming angiotensin II, which inhibits downstream effects.
ARBs
Angiotensin II receptor blockers (ARBs) have a similar effect as ACE inhibitors because they also block the downstream response of the renin-angiotensin-aldosterone system.
As the name suggests, angiotensin II receptor blockers block angiotensin II receptors.
In other words they are angiotensin II receptor antagonists.
We can again see the renin-angiotensin-aldosterone system below.
However, we are not inhibiting angiotensin-converting enzyme like we saw with ACE inhibitors. Instead we are blocking the angiotensin II receptors.
If angiotensin II is unable to bind to its receptors, then the downstream effects that would normally increase blood pressure will not occur.
This can help control high blood pressure as a result.
For more information about the mechanism of action, indications, side effects, and contraindications of ARBs, check out the Angiotensin II Receptor Blockers lecture.
ARB Mechanism of Action: Blocks angiotensin II receptors, which blocks the downstream effects of angiotensin II
Alpha Blockers
The next class of antihypertensive medications is alpha blockers.
The mechanism of action is self explanatory by their name as they block alpha receptors.
In other words, alpha blockers are alpha receptor antagonists.
Alpha blockers lower blood pressure primarily by blocking the alpha-1 receptors on blood vessels.
You might remember alpha receptors are a type of adrenergic receptor that play a role in our sympathetic nervous system, which is our flight or fight response when we are in stressful or dangerous situations.
One of those responses is to increase blood pressure in order to perfuse our vital tissues and organs.
We can do this by activating the alpha-1 receptors on blood vessels.
Sympathetic catecholamines such as norepinephrine and epinephrine increase during a sympathetic response, and they can bind to alpha-1 receptors on blood vessels.
Norepinephrine has a higher affinity compared to epinephrine, however they both can bind to alpha-1 receptors and activate them.
Activation of the alpha-1 receptors on blood vessels causes vascular smooth muscle contraction and vasoconstriction to occur, leading to an increase in blood pressure.
Vascular Alpha-1 Receptors: Sympathetic catecholamines such as norepinephrine and epinephrine can bind to alpha-1 receptors on blood vessels to increase vasoconstriction and blood pressure.
Alpha blockers lower blood pressure primarily by blocking the sympathetic activation of alpha-1 receptors on blood vessels.
If we block alpha-1 receptors on blood vessels using an alpha blocker, then norepinephrine and epinephrine have difficulty binding to the receptor.
Vasoconstriction will decrease, and this will help to control high blood pressure as a result.
There are different types of alpha blockers, including selective and nonselective, depending on if they bind to alpha-1 receptors, alpha-2 receptors, or both. This will be discussed more in the alpha antagonist post.
Alpha Blocker Mechanism of Action: Blocks alpha-1 receptors on blood vessels, thereby preventing sympathetic catecholamines such as norepinephrine and epinephrine from binding. This causes decreased vasoconstriction and blood pressure.
If you want to learn more about the different types of alpha receptors, where they’re located in the body, and what their effects are, all of that can be found in the following post:
“Adrenergic Receptors: Team Alpha”
For more information about the autonomic nervous system and the sympathetic fight or flight response, make sure to check out:
Beta Blockers
Now that we understand alpha blockers, let’s talk about how beta blockers control high blood pressure.
As the name suggests, they block beta receptors.
In other words, beta blockers are beta receptor antagonists.
Similar to alpha receptors, beta receptors are also a type of adrenergic receptor activated by catecholamines from the sympathetic nervous system.
Again, in a sympathetic fight or flight response we increase blood pressure in order to perfuse vital tissues and organs.
We already know from above that alpha-1 receptors on blood vessels can increase blood pressure through vasoconstriction.
There are beta receptors in the heart that can increase blood pressure when activated too.
When sympathetic catecholamines such as norepinephrine and epinephrine bind to beta-1 receptors in the heart, heart rate increases (chronotropy) and stroke volume increases from increased cardiac contraction (inotropy).
Increased heart rate and stroke volume will lead to an increase in cardiac output, which will lead to an increase in blood pressure as a result.
Remember blood pressure (BP) equals cardiac output (CO) times systemic vascular resistance (SVR), also known as total peripheral resistance.
BP = CO x SVR
Cardiac output is also equal to heart rate (HR) times stroke volume (SV).
CO = HR x SV
We will discuss these equations more in the next section when we review the last column of the chart.
Cardiac Beta-1 Receptors: Sympathetic catecholamines such as norepinephrine and epinephrine can bind to beta-1 receptors in the heart to increase heart rate (HR), stroke volume (SV), cardiac output (CO), and blood pressure (BP).
Beta blockers lower blood pressure primarily by blocking the sympathetic activation of beta-1 receptors in the heart.
If we use beta blockers to block the beta-1 receptors, then norepinephrine and epinephrine will have difficulty binding.
Heart rate and stroke volume decrease, thereby decreasing cardiac output and blood pressure as a result.
Similar to alpha blockers, there are selective and nonselective beta blockers, depending on whether they bind to one or more types of beta receptors. This will be discussed more in the beta antagonist lecture.
If you want to learn more about the different types of beta receptors, where they’re located, and what their effects are, all of that can be found in the following post:
Beta Blocker Mechanism of Action: Blocks beta-1 receptors in the heart, thereby preventing sympathetic catecholamines such as norepinephrine and epinephrine from binding. This causes decreased heart rate, stroke volume, cardiac output, and blood pressure.
Calcium Channel Blockers
The next class of antihypertensives is calcium channel blockers.
The name is again self-explanatory as they block calcium channels located on vascular smooth muscles cells and cardiac muscle cells.
There are 2 main types of calcium channel blockers based on their main site of action.
They are known as dihydropyridines and non-dihydropyridines.
Dihydropyridines predominately act on blood vessels with less of an effect on the heart, while non-dihydropyridines act mainly on the heart with less of an effect on blood vessels.
The dihydropyridines block calcium channels located on the smooth muscle of blood vessels thereby causing vasodilation, whereas non-dihydropyridines block calcium channels in the heart thereby causing decreased heart rate and cardiac contraction.
As a result, dihydropyridines are more common for hypertension and non-dihydropyridines are more common for tachydysrhythmias but can still affect blood pressure as well.
Calcium Channel Blockers: Dihydropyridines predominately target calcium channels of blood vessels and cause vasodilation to treat hypertension. Non-dihydropyridines predominately target calcium channels of the heart and cause decreased heart rate and cardiac contraction to treat tachydysrhythmias.
Dihydropyridines
Since antihypertensives are the focus of this lecture, let’s take a closer look at dihydropyridines as they are more commonly used for hypertension.
There are calcium channels located on the smooth muscle cells of blood vessels.
When calcium enters the cells via calcium channels, it will lead to smooth muscle contraction and vasoconstriction.
As we know from above, vasoconstriction increases systemic vascular resistance which will increase blood pressure.
Vascular Smooth Muscle Cell Calcium Channels: When calcium enters vascular smooth muscle cells through calcium channels, it leads to smooth muscle contraction, vasoconstriction, and an increase in blood pressure.
If we block calcium channels with a calcium channel blocker, then we will decrease the influx of calcium into the smooth muscle cells, thereby decreasing smooth muscle contraction and vasoconstriction, and ultimately decreasing blood pressure.
Dihydropyridine Calcium Channel Blockers: Dihydropyridines mainly block the calcium channels of vascular smooth muscle cells, thereby preventing the influx of calcium. This decreases smooth muscle contraction, vasoconstriction, and blood pressure.
Non-Dihydropyridines
The mechanism of action for non-dihydropyridines is similar, but they primarily block the influx of calcium into cardiac muscle cells (myocytes).
Normally the influx of calcium into cardiac myocytes will increase the automaticity and conduction velocity of pacemaker cells, thereby increasing heart rate.
Calcium also increases the force of contraction of non-pacemaker contractile cells (atrial and ventricular cardiac myocytes), thereby increasing stroke volume.
Cardiac Muscle Cell Calcium Channels: When calcium enters cardiac muscle cells through calcium channels, it leads to increased heart rate and cardiac contraction.
Blocking cardiac calcium channels with non-dihydropyridines will decrease heart rate and cardiac contraction for the reasons mentioned above.
Therefore, calcium channel blockers (particularly the non-dihydropyridines) are a class of antiarrhythmic drugs, and can also decrease blood pressure.
Antiarrhythmic drugs are made easy using this “Antiarrhythmic Mnemonic”.
We will discuss calcium channel blockers in more detail in the calcium channel blocker post.
Non-Dihydropyridine Calcium Channel Blockers: Non-Dihydropyridines mainly block the calcium channels of cardiac muscle cells, thereby preventing the influx of calcium. This decreases heart rate and cardiac contraction.
Diuretics
The final major class of antihypertensive medications is diuretics.
As the name suggests, diuretics will facilitate diuresis in the kidneys.
You might recall the kidney is composed of functional units called nephrons that work to reabsorb, secrete, and excrete various substances.
One of the functions of the nephron is to regulate sodium and water reabsorption.
Water generally follows sodium. If we reabsorb sodium, then we will retain more water which will increase our circulating plasma volume in our blood vessels.
This will increase blood pressure as a result.
Diuretics act on various parts of the nephron depending on the diuretic used.
However, the general concept of controlling blood pressure is similar among all diuretics.
The general mechanism of action is to inhibit water reabsorption, thereby increasing water excretion or diuresis.
The decreased water reabsorption decreases plasma volume, which will decrease blood pressure.
Diuretic Mechanism of Action: Diuretics facilitate diuresis mainly by blocking sodium and/or water reabsorption in the nephron of the kidney. The increase in diuresis decreases plasma volume, stroke volume, and blood pressure.
Effects on Blood Pressure
Now that we know the mechanism of action for each antihypertensive class, we can figure out which blood pressure variables are involved.
Antihypertensive Medications: Main Effect on Blood Pressure (BP)
Blood Pressure Variables
Remember blood pressure equals cardiac output times systemic vascular resistance, also known as total peripheral resistance.
BP = CO x SVR
Cardiac output can be broken down further into heart rate times stroke volume.
CO = HR x SV
In other words blood pressure is equal to heart rate times stroke volume times systemic vascular resistance.
BP = HR x SV x SVR
Blood Pressure and Cardiac Output Equations: BP = Blood Pressure; CO = Cardiac Output; SVR = Systemic Vascular Resistance; TPR = Total Peripheral Resistance; HR = Heart Rate; SV = Stroke Volume
Effects on Blood Pressure
Let’s look at which blood pressure variable(s) are involved for each antihypertensive class.
ACE Inhibitors
The major blood pressure variables impacted by ACE inhibitors are systemic vascular resistance (SVR) and stroke volume (SV).
ACE inhibitors decrease both SVR and SV.
We know ACE inhibitors block angiotensin converting enzyme from converting angiotensin I into angiotensin II.
Decreased angiotensin II levels will lead to a decrease in vasoconstriction and a decrease in SVR as a result.
Angiotensin II also increases sodium and water reabsorption in the kidneys, as well as augments aldosterone and antidiuretic hormone release which both function to reabsorb sodium/water.
Decreased levels of angiotensin II from an ACE inhibitor will lead to a decrease in sodium/water reabsorption, which will decrease blood volume, which will decrease SV.
ARBs
ARBs block angiotensin II receptors and will have a similar effect as ACE inhibitors.
We will see a decrease in systemic vascular resistance (SVR) and stroke volume (SV).
Alpha Blockers
The major blood pressure variable impacted by alpha blockers is systemic vascular resistance (SVR).
We learned alpha blockers decrease blood pressure primarily by blocking alpha-1 receptors on blood vessels.
This will decrease vasoconstriction and SVR.
Beta Blockers
The major blood pressure variables impacted by beta blockers are heart rate (HR) and stroke volume (SV).
We know beta blockers will decrease blood pressure primarily by blocking beta-1 receptors in the heart.
This will decrease HR and SV (due to decreased cardiac contraction).
Decreasing HR and SV decreases cardiac output (CO), which will decrease blood pressure.
Calcium Channel Blockers
The major blood pressure variables impacted by calcium channel blockers are systemic vascular resistance (SVR), heart rate (HR), and stroke volume (SV).
The dihydropyridine calcium channel blockers lower blood pressure primarily by blocking calcium channels on blood vessels.
This will decrease vascular smooth muscle contraction, which will decrease vasoconstriction, which will decrease SVR as a result.
We also know the non-dihydropyridines predominantly act on cardiac muscle cells.
Although used more for tachydysrhythmias, non-dihydropyridines can also decrease blood pressure by lowering HR, as well as SV from decreased cardiac contraction.
Diuretics
The major blood pressure variable impacted by diuretics is stroke volume (SV).
Diuretics ultimately decrease plasma volume by inhibiting water reabsorption in the kidneys.
The decrease in circulating plasma volume will decrease SV.
Antihypertensive Medications: Effect on Blood Pressure Variables
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