Understanding Anti-Hypertensive Medications

Welcome back to the EasyMed channel where medical and science topics are made easy. This video will be an overview to anti-hypertensive medications which are used to treat high blood pressure. In the next 15 or 16 minutes you're going to save yourself a lot of time in studying. You'll learn the main classes of antihypertensives along with tricks to remember what those classes are and several tricks to remember the drug names, example medications, and mechanism of action of each class. I also made this chart to make it easy for you and by the end of this video you'll know everything shown. So make sure to watch the entire video as it will save you a lot of time studying and reviewing. Let's first start by giving you a trick to remember the main antihypertensive classes. Antihypertensive medications are used to treat high blood pressure, also known as hypertension. The easy way to remember the main antihypertensive classes is to use ABCD. A will stand for several different antihypertensive medications, the first one being angiotensin converting enzyme inhibitors, also known as ACE inhibitors. The second A stands for angiotensin 2 receptor blockers, also known as ARBs, and the final A stands for alpha blockers. Moving on to B, this will help you remember beta blockers, The C will stand for calcium channel blockers. Finally, the D is to help you remember diuretics. While there are other antihypertensive medications out there, these are the main ones and generally the more common ones. You might also learn about central agonists and vasodilators. You can use the C to remember central agonists and you can use the D to remember dilators for vasodilators. So as you can see, this gives you a great way to organize the main antihypertensive drug classes. So write this down and keep it in your notes. Now that we've learned an easy way to remember the main classes shown in the first column, let's learn an easy way to remember the drug names within each class. There's a simple trick for this using the suffix of each medication. ACE inhibitors usually end in pril. ARBs typically have the suffix sartin. Alpha blockers end in osin. And many of the alpha blockers specific to treating hypertension end in zosin with a z. The suffix osin or zosin apply to selective alpha-1 blockers. There are also non-selective alpha-1 and alpha-2 blockers and they typically end in mean or mined. Some examples include phentalamine and phenoxybenzamine. They're usually considered in treating pheochromocytoma and cocaine-induced hypertension, but since they're used more for catecholamine-induced hypertension, we'll focus on selective alpha-1 antagonists for purposes of this video. The alpha blocker video will go into more detail on both the selective and non-selective types of alpha blockers. So just make sure you're aware that osonin applies to selective alpha-1 blockers. Moving on to beta blockers, they have the suffix lol, and many of the calcium channel blockers end in dipine or dipine, especially dihydropyridines. There are two main types of calcium channel blockers, dihydropyridines and non-dihydropyridines. Generally speaking, dihydropyridines are used more for hypertension as they target blood vessels, while non-dihydropyridines such as verapamil and diltiazem are used for the blood vessels. are used more for tachydysrhythmias as they target the heart. Since the dihydropyridines are used more for blood pressure, we'll be focusing on those in this video. But the calcium channel blocker video will go into more detail about both types. So just know the suffix dipine or dipine applies to the dihydropyridine calcium channel blockers. As we move on to diuretics, many of these medications end with"-ide". For the most part, using these suffixes will be a great way to remember most of the drug names within each class. Just know that there are some exceptions out there and this isn't a hard fast rule. Now that we have an easy way to remember the drug names within each class, let's take a look at some examples. We know ACE inhibitors end in pril. Some examples include lisinopril and enalapril. ARBs have the suffix sartin and some examples are losartin and valsartin. Alpha blockers, specifically the selective alpha-1 blockers, end in osin such as doxazosin and terezosin, also pronounced terezosin. Example beta blockers include metoprolol and labetalol, and you can see how they end in LOL. The dihydropyridine calcium channel blockers typically end in dipine, such as amlodipine and nicardipine. Finally, many but not all diuretics end in IID, as we can see with furosemide and hydrochlorothiazide. As we continue to work our way through the chart, let's take a look at the mechanism of action of each antihypertensive class. This will help us get a better understanding as to how the medications are used to lower blood pressure. Starting with ACE inhibitors, as the name suggests, they're going to inhibit angiotensin-converting enzyme, also known as ACE. Remember, angiotensin-converting enzyme is a part of the renin-angiotensin-aldosterone system. Specifically, it's involved in converting angiotensin-1 into angiotensin-2. Angiotensin-2 is the active hormone involved in increasing blood pressure through a number of mechanisms. Angiotensin 2 can bind to angiotensin receptors on blood vessels, which leads to vasoconstriction and this increases blood pressure. Angiotensin 2 also increases reabsorption of sodium and water in the kidneys and augments the release of aldosterone from the adrenal cortex and the release of antidiuretic hormone from the posterior pituitary gland and all of this will work to increase blood pressure. Well if we block angiotensin converting enzyme then we will decrease the formation of angiotensin 2. Without angiotensin 2 we won't have the downstream effects of raising blood pressure. This can control high blood pressure as a result. There's a previous EasyMed video on the renin-angiotensin-aldosterone system if you want more information on this. It's linked down below in the description. Angiotensin-2 receptor blockers, also known as ARBs, have a similar effect as ACE inhibitors because they're also blocking the renin-angiotensin-aldosterone system. As the name suggests, angiotensin-2 receptor blockers will block angiotensin-2 receptors. In other words, they're angiotensin-2 receptor antagonists. Again, we can see the renin-angiotensin-aldosterone system. This time, however, we're not inhibiting angiotensin-converting enzyme, but we're blocking the angiotensin-2 receptors. If angiotensin-2 can't bind to its receptors, then we won't have the downstream effects we talked about earlier that would normally increase blood pressure. Moving on to alpha blockers, the mechanism of action is self-explanatory by their name. They're going to block alpha receptors. In other words, they're alpha receptor antagonists. Alpha blockers lower blood pressure primarily by blocking the alpha-1 receptors on blood vessels. Alpha receptors are a type of adrenergic receptor that play a role in our sympathetic nervous system, which is our fight-or-flight response when we're 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 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 these alpha-1 receptors on blood vessels causes vascular smooth muscle contraction and vasoconstriction occurs, leading to an increase in 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 alpha blockers, then norepinephrine and epinephrine can't bind 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 non-selective, depending on if they bind to alpha-1 receptors, alpha-2 receptors, or both. This will be discussed more in the alpha antagonist video. 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 that can be found in the alpha receptor EZMed video linked below. There's also an EZMed autonomic nervous system video linked in the description if you want more information on the sympathetic nervous system. Now that we understand alpha blockers, let's talk about how beta blockers control high blood pressure. As the name suggests, they're going to block beta receptors. In other words, they're beta receptor antagonists. Similar to alpha receptors, beta receptors are also a type of adrenergic receptor activated by catecholamines from the sympathetic fight-or-flight response. Again, in a sympathetic response, we increase blood pressure to perfuse vital tissues and organs. We already learned how alpha-1 receptors on blood vessels increase blood pressure through vasoconstriction, but there are beta receptors in the heart that 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, as well as stroke volume increases from increased cardiac contraction. This will cause increased cardiac output and increased blood pressure as a result. Remember, blood pressure equals cardiac output times systemic vascular resistance, also known as total peripheral resistance. Cardiac output is equal to heart rate times stroke volume. So you can see if we increase heart rate and stroke volume, the cardiac output will increase, which will in turn increase blood pressure. We'll talk more about these equations in a bit when we get to the final column of the chart. 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 these beta-1 receptors, the norepinephrine and epinephrine can't bind. Heart rate and stroke volume decrease, thereby decreasing cardiac output, and blood pressure is controlled as a result. Similar to alpha blockers, there are selective and non-selective forms of beta blockers. depending on whether they bind to one or more types of beta receptors. This will be discussed more in the beta antagonist video. And if you want to learn more information about the different types of beta receptors, where they're located in the body, and what their effects are, all that can be found in the beta receptor easymed video linked below. The next antihypertensive class is calcium channel blockers. The name again is self-explanatory as they're going to block calcium channels primarily located on vascular smooth muscle cells and cardiac muscle cells. There are two main types of calcium channel blockers based on their main side of action. They're known as dihydropyridines and non-dihydropyridines. Dihydropyridines predominantly 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. Dihydropyridines cause vasodilation by blocking calcium channels located on blood vessels, whereas non-dihydropyridines decrease heart rate and cardiac contraction by blocking calcium channels located in the heart. As a result, dihydropyridines are more common for hypertension and non-dihydropyridines are used more for tachydysrhythmias, but they can still have an effect on blood pressure as well. Since we're focusing on antihypertensives in this video, Let's take a closer look at dihydropyridines as they're more common for hypertension. There are calcium channels located on the smooth muscle cells of blood vessels. When calcium enters the cells through the calcium channels, it will lead to smooth muscle contraction and vasoconstriction. As we know from before, vasoconstriction will cause blood pressure to increase. If we block calcium channels with calcium channel blockers, then we will decrease the influx of calcium into smooth muscle cells. This will decrease smooth muscle contraction and vasoconstriction, and ultimately decrease blood pressure. The mechanism of action for non-dihydropyridines is similar, but they're going to block the influx of calcium into cardiac muscle cells. This will decrease heart rate and cardiac contractility. For this reason, calcium channel blockers are also a type of antiarrhythmic drug, particularly the non-dihydropyridines. You can learn more about antiarrhythmics in the EasyMed video linked below. The final main class of antihypertensives is diuretics. As the name suggests, diuretics will facilitate diuresis in the kidneys. Remember, the kidney is made up 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, so if we reabsorb sodium, then we're going to retain more water. This will increase our circulating plasma volume in our blood vessels. and will increase blood pressure as a result. Diuretics act on various parts of the nephron depending on which diuretic it is. However, the general concept is the same among diuretics when it comes to controlling blood pressure. Their general mechanism of action is to inhibit or decrease water reabsorption and or sodium reabsorption. This will increase water excretion or diuresis. Since we're retaining less water, the plasma volume is decreased and this will ultimately decrease blood pressure. Now that we have a good understanding of the mechanism of action of each antihypertensive class, we can now figure out the main effects they'll have on blood pressure. Remember we said earlier blood pressure equals cardiac output times systemic vascular resistance, also known as total peripheral resistance. Cardiac output can be broken down further into heart rate times stroke volume. In other words, blood pressure is equal to heart rate times stroke volume times systemic vascular resistance. Let's see what parts of the equation each class primarily affects. We know ACE inhibitors inhibit angiotensin-converting enzyme from forming angiotensin-2. Angiotensin-2 likes to bind to blood vessels, which causes vasoconstriction. So with lower levels of angiotensin-2, we're not going to get as much vasoconstriction, and this will decrease systemic vascular resistance. ACE inhibitors will also decrease stroke volume. Remember, angiotensin-2 augments sodium and water reabsorption in the kidneys, and also augments the release of aldosterone and antidiuretic hormone. Both of these will increase sodium and water reabsorption in the kidney as well. So you can see that will impact stroke volume. ARBs block angiotensin 2 receptors and will have a similar effect as ACE inhibitors. We will see a decrease in systemic vascular resistance and stroke volume. We know alpha blockers decrease blood pressure primarily by blocking alpha-1 receptors on blood vessels. This will decrease vasoconstriction and systemic vascular resistance. We know beta blockers will decrease blood pressure primarily by blocking beta-1 receptors in the heart. This will decrease heart rate as well as stroke volume due to decreased cardiac contraction. Calcium channel blockers lower blood pressure primarily by blocking calcium channels on blood vessels, particularly the dihydropyridines. This will decrease vascular smooth muscle contraction, vasoconstriction, and systemic vascular resistance as a result. We also know the non-dihydropyridines predominantly act on calcium channels of cardiac muscle cells. Although used more for tachydysrhythmias, this can also decrease blood pressure by decreasing heart rate, as well as stroke volume from decreased cardiac contraction. Finally, we have diuretics which ultimately decrease plasma volume by inhibiting water reabsorption in the kidneys. This decrease in circulating plasma volume will decrease stroke volume. You should now have a good understanding of this chart. As always, you can find this chart here. and all of the notes for this video on the EasyMed website, easymedlearning.com. It'll be linked down below in the description. Hopefully this was a good overview of the main antihypertensive classes. If you found this useful in any way, please give it a quick like or comment down below. It truly helps. And if you're new to the channel, make sure to subscribe. That way you don't miss out on future videos that make medical and science topics easy, especially the videos that will go in more detail on each antihypertensive class. Thanks for watching and I hope you check out future videos.

You'll learn the main classes of antihypertensives along with tricks to remember what those classes are and several tricks to remember the drug names, example medications, and mechanism of action of each class. I also made this chart to make it easy for you and by the end of this video you'll know everything shown. So make sure to watch the entire video as it will save you a lot of time studying and reviewing. Let's first start by giving you a trick to remember the main antihypertensive classes.

Antihypertensive medications are used to treat high blood pressure, also known as hypertension. The easy way to remember the main antihypertensive classes is to use ABCD. A will stand for several different antihypertensive medications, the first one being angiotensin converting enzyme inhibitors, also known as ACE inhibitors. The second A stands for angiotensin 2 receptor blockers, also known as ARBs, and the final A stands for alpha blockers.

Moving on to B, this will help you remember beta blockers, The C will stand for calcium channel blockers. Finally, the D is to help you remember diuretics. While there are other antihypertensive medications out there, these are the main ones and generally the more common ones.

You might also learn about central agonists and vasodilators. You can use the C to remember central agonists and you can use the D to remember dilators for vasodilators. So as you can see, this gives you a great way to organize the main antihypertensive drug classes. So write this down and keep it in your notes.

Now that we've learned an easy way to remember the main classes shown in the first column, let's learn an easy way to remember the drug names within each class. There's a simple trick for this using the suffix of each medication. ACE inhibitors usually end in pril.

ARBs typically have the suffix sartin. Alpha blockers end in osin. And many of the alpha blockers specific to treating hypertension end in zosin with a z. The suffix osin or zosin apply to selective alpha-1 blockers.

There are also non-selective alpha-1 and alpha-2 blockers and they typically end in mean or mined. Some examples include phentalamine and phenoxybenzamine. They're usually considered in treating pheochromocytoma and cocaine-induced hypertension, but since they're used more for catecholamine-induced hypertension, we'll focus on selective alpha-1 antagonists for purposes of this video.

The alpha blocker video will go into more detail on both the selective and non-selective types of alpha blockers. So just make sure you're aware that osonin applies to selective alpha-1 blockers. Moving on to beta blockers, they have the suffix lol, and many of the calcium channel blockers end in dipine or dipine, especially dihydropyridines.

There are two main types of calcium channel blockers, dihydropyridines and non-dihydropyridines. Generally speaking, dihydropyridines are used more for hypertension as they target blood vessels, while non-dihydropyridines such as verapamil and diltiazem are used for the blood vessels. are used more for tachydysrhythmias as they target the heart.

Since the dihydropyridines are used more for blood pressure, we'll be focusing on those in this video. But the calcium channel blocker video will go into more detail about both types. So just know the suffix dipine or dipine applies to the dihydropyridine calcium channel blockers. As we move on to diuretics, many of these medications end with"-ide".

For the most part, using these suffixes will be a great way to remember most of the drug names within each class. Just know that there are some exceptions out there and this isn't a hard fast rule. Now that we have an easy way to remember the drug names within each class, let's take a look at some examples. We know ACE inhibitors end in pril. Some examples include lisinopril and enalapril.

ARBs have the suffix sartin and some examples are losartin and valsartin. Alpha blockers, specifically the selective alpha-1 blockers, end in osin such as doxazosin and terezosin, also pronounced terezosin. Example beta blockers include metoprolol and labetalol, and you can see how they end in LOL. The dihydropyridine calcium channel blockers typically end in dipine, such as amlodipine and nicardipine.

Finally, many but not all diuretics end in IID, as we can see with furosemide and hydrochlorothiazide. As we continue to work our way through the chart, let's take a look at the mechanism of action of each antihypertensive class. This will help us get a better understanding as to how the medications are used to lower blood pressure. Starting with ACE inhibitors, as the name suggests, they're going to inhibit angiotensin-converting enzyme, also known as ACE.

Remember, angiotensin-converting enzyme is a part of the renin-angiotensin-aldosterone system. Specifically, it's involved in converting angiotensin-1 into angiotensin-2. Angiotensin-2 is the active hormone involved in increasing blood pressure through a number of mechanisms.

Angiotensin 2 can bind to angiotensin receptors on blood vessels, which leads to vasoconstriction and this increases blood pressure. Angiotensin 2 also increases reabsorption of sodium and water in the kidneys and augments the release of aldosterone from the adrenal cortex and the release of antidiuretic hormone from the posterior pituitary gland and all of this will work to increase blood pressure. Well if we block angiotensin converting enzyme then we will decrease the formation of angiotensin 2. Without angiotensin 2 we won't have the downstream effects of raising blood pressure. This can control high blood pressure as a result. There's a previous EasyMed video on the renin-angiotensin-aldosterone system if you want more information on this.

It's linked down below in the description. Angiotensin-2 receptor blockers, also known as ARBs, have a similar effect as ACE inhibitors because they're also blocking the renin-angiotensin-aldosterone system. As the name suggests, angiotensin-2 receptor blockers will block angiotensin-2 receptors.

In other words, they're angiotensin-2 receptor antagonists. Again, we can see the renin-angiotensin-aldosterone system. This time, however, we're not inhibiting angiotensin-converting enzyme, but we're blocking the angiotensin-2 receptors. If angiotensin-2 can't bind to its receptors, then we won't have the downstream effects we talked about earlier that would normally increase blood pressure.

Moving on to alpha blockers, the mechanism of action is self-explanatory by their name. They're going to block alpha receptors. In other words, they're alpha receptor antagonists.

Alpha blockers lower blood pressure primarily by blocking the alpha-1 receptors on blood vessels. Alpha receptors are a type of adrenergic receptor that play a role in our sympathetic nervous system, which is our fight-or-flight response when we're 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 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 these alpha-1 receptors on blood vessels causes vascular smooth muscle contraction and vasoconstriction occurs, leading to an increase in 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 alpha blockers, then norepinephrine and epinephrine can't bind 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 non-selective, depending on if they bind to alpha-1 receptors, alpha-2 receptors, or both.

This will be discussed more in the alpha antagonist video. 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 that can be found in the alpha receptor EZMed video linked below.

There's also an EZMed autonomic nervous system video linked in the description if you want more information on the sympathetic nervous system. Now that we understand alpha blockers, let's talk about how beta blockers control high blood pressure. As the name suggests, they're going to block beta receptors.

In other words, they're beta receptor antagonists. Similar to alpha receptors, beta receptors are also a type of adrenergic receptor activated by catecholamines from the sympathetic fight-or-flight response. Again, in a sympathetic response, we increase blood pressure to perfuse vital tissues and organs.

We already learned how alpha-1 receptors on blood vessels increase blood pressure through vasoconstriction, but there are beta receptors in the heart that 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, as well as stroke volume increases from increased cardiac contraction. This will cause increased cardiac output and increased blood pressure as a result. Remember, blood pressure equals cardiac output times systemic vascular resistance, also known as total peripheral resistance. Cardiac output is equal to heart rate times stroke volume.

So you can see if we increase heart rate and stroke volume, the cardiac output will increase, which will in turn increase blood pressure. We'll talk more about these equations in a bit when we get to the final column of the chart. 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 these beta-1 receptors, the norepinephrine and epinephrine can't bind. Heart rate and stroke volume decrease, thereby decreasing cardiac output, and blood pressure is controlled as a result.

Similar to alpha blockers, there are selective and non-selective forms of beta blockers. depending on whether they bind to one or more types of beta receptors. This will be discussed more in the beta antagonist video.

And if you want to learn more information about the different types of beta receptors, where they're located in the body, and what their effects are, all that can be found in the beta receptor easymed video linked below. The next antihypertensive class is calcium channel blockers. The name again is self-explanatory as they're going to block calcium channels primarily located on vascular smooth muscle cells and cardiac muscle cells.

There are two main types of calcium channel blockers based on their main side of action. They're known as dihydropyridines and non-dihydropyridines. Dihydropyridines predominantly 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.

Dihydropyridines cause vasodilation by blocking calcium channels located on blood vessels, whereas non-dihydropyridines decrease heart rate and cardiac contraction by blocking calcium channels located in the heart. As a result, dihydropyridines are more common for hypertension and non-dihydropyridines are used more for tachydysrhythmias, but they can still have an effect on blood pressure as well. Since we're focusing on antihypertensives in this video, Let's take a closer look at dihydropyridines as they're more common for hypertension.

There are calcium channels located on the smooth muscle cells of blood vessels. When calcium enters the cells through the calcium channels, it will lead to smooth muscle contraction and vasoconstriction. As we know from before, vasoconstriction will cause blood pressure to increase. If we block calcium channels with calcium channel blockers, then we will decrease the influx of calcium into smooth muscle cells. This will decrease smooth muscle contraction and vasoconstriction, and ultimately decrease blood pressure.

The mechanism of action for non-dihydropyridines is similar, but they're going to block the influx of calcium into cardiac muscle cells. This will decrease heart rate and cardiac contractility. For this reason, calcium channel blockers are also a type of antiarrhythmic drug, particularly the non-dihydropyridines.

You can learn more about antiarrhythmics in the EasyMed video linked below. The final main class of antihypertensives is diuretics. As the name suggests, diuretics will facilitate diuresis in the kidneys.

Remember, the kidney is made up 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, so if we reabsorb sodium, then we're going to retain more water. This will increase our circulating plasma volume in our blood vessels. and will increase blood pressure as a result.

Diuretics act on various parts of the nephron depending on which diuretic it is. However, the general concept is the same among diuretics when it comes to controlling blood pressure. Their general mechanism of action is to inhibit or decrease water reabsorption and or sodium reabsorption. This will increase water excretion or diuresis. Since we're retaining less water, the plasma volume is decreased and this will ultimately decrease blood pressure.

Now that we have a good understanding of the mechanism of action of each antihypertensive class, we can now figure out the main effects they'll have on blood pressure. Remember we said earlier blood pressure equals cardiac output times systemic vascular resistance, also known as total peripheral resistance. Cardiac output can be broken down further into heart rate times stroke volume.

In other words, blood pressure is equal to heart rate times stroke volume times systemic vascular resistance. Let's see what parts of the equation each class primarily affects. We know ACE inhibitors inhibit angiotensin-converting enzyme from forming angiotensin-2.

Angiotensin-2 likes to bind to blood vessels, which causes vasoconstriction. So with lower levels of angiotensin-2, we're not going to get as much vasoconstriction, and this will decrease systemic vascular resistance. ACE inhibitors will also decrease stroke volume. Remember, angiotensin-2 augments sodium and water reabsorption in the kidneys, and also augments the release of aldosterone and antidiuretic hormone. Both of these will increase sodium and water reabsorption in the kidney as well.

So you can see that will impact stroke volume. ARBs block angiotensin 2 receptors and will have a similar effect as ACE inhibitors. We will see a decrease in systemic vascular resistance and stroke volume. We know alpha blockers decrease blood pressure primarily by blocking alpha-1 receptors on blood vessels.

This will decrease vasoconstriction and systemic vascular resistance. We know beta blockers will decrease blood pressure primarily by blocking beta-1 receptors in the heart. This will decrease heart rate as well as stroke volume due to decreased cardiac contraction. Calcium channel blockers lower blood pressure primarily by blocking calcium channels on blood vessels, particularly the dihydropyridines. This will decrease vascular smooth muscle contraction, vasoconstriction, and systemic vascular resistance as a result.

We also know the non-dihydropyridines predominantly act on calcium channels of cardiac muscle cells. Although used more for tachydysrhythmias, this can also decrease blood pressure by decreasing heart rate, as well as stroke volume from decreased cardiac contraction. Finally, we have diuretics which ultimately decrease plasma volume by inhibiting water reabsorption in the kidneys. This decrease in circulating plasma volume will decrease stroke volume.

You should now have a good understanding of this chart. As always, you can find this chart here. and all of the notes for this video on the EasyMed website, easymedlearning.com. It'll be linked down below in the description.

Hopefully this was a good overview of the main antihypertensive classes. If you found this useful in any way, please give it a quick like or comment down below. It truly helps.

And if you're new to the channel, make sure to subscribe. That way you don't miss out on future videos that make medical and science topics easy, especially the videos that will go in more detail on each antihypertensive class. Thanks for watching and I hope you check out future videos.

Transcript for:Understanding Anti-Hypertensive Medications

Transcript for:
Understanding Anti-Hypertensive Medications