Pharmacology - HYPERTENSION & ANTIHYPERTENSIVES (MADE EASY)

Summary

This lecture delves into the pharmacology of antihypertensive drugs, explaining the physiological basis of blood pressure regulation and the role of systems like baroreceptors and the renin-angiotensin-aldosterone system. It outlines various drug classes that target these mechanisms, such as alpha-1 blockers, beta blockers, calcium channel blockers, diuretics, and drugs affecting the renin-angiotensin-aldosterone system, to reduce blood pressure. The lecture also touches on side effects and other agents like Bosentan and Fenoldopam, providing a comprehensive overview of hypertension management.

Takeaways

• 💡 Hypertension is a common disorder often without noticeable symptoms and is related to the force of blood against artery walls.
• 🌡 Blood pressure is maintained by factors such as cardiac output, systemic vascular resistance, arterial wall elasticity, and blood volume.
• 🔍 Baroreceptors in the aortic arch and carotid sinuses are key in blood pressure regulation, responding to changes and triggering the release of catecholamines.
• 🏋️‍♂️ Beta-1 receptor activation increases heart rate and stroke volume, boosting cardiac output and blood pressure.
• 🌀 Alpha-1 receptor activation leads to vasoconstriction, increasing vascular resistance and blood pressure.
• 🚰 The renin-angiotensin-aldosterone system plays a significant role in blood pressure regulation, with renin initiating the production of angiotensin II, a potent vasoconstrictor.
• 🛡️ Antihypertensive drugs work by disrupting different aspects of the blood pressure regulation system, with classes including alpha-1 blockers, beta blockers, and others.
• 💊 Alpha-1 blockers like Doxazosin reduce systemic vascular resistance and blood pressure by blocking alpha-1 receptors on smooth muscle.
• 💓 Selective beta blockers such as Atenolol decrease cardiac output by blocking beta-1 receptors on the heart, thus lowering blood pressure.
• 🧠 Centrally acting adrenergic drugs like Clonidine work by reducing sympathetic activity in the brain, leading to decreased blood pressure.
• 💊 Calcium channel blockers, divided into dihydropyridines and nondihydropyridines, reduce blood pressure by inhibiting calcium entry into smooth muscle cells or cardiac cells, respectively.
• 🌿 Diuretics are categorized into loop, thiazide, and potassium-sparing, each reducing blood pressure through different mechanisms involving sodium and water balance in the body.
• 🛑 Drugs targeting the renin-angiotensin-aldosterone system, such as renin inhibitors, ACE inhibitors, and ARBs, lower blood pressure by reducing angiotensin II production or its effects.
• 🚑 Other antihypertensive agents not fitting into the main classes include Bosentan for pulmonary hypertension, Fenoldopam for short-term severe hypertension management, and direct-acting smooth muscle relaxants like Hydralazine.

Q & A

What is hypertension and why is it often asymptomatic?

Hypertension, also known as high blood pressure, is a common disorder that affects many people. It is often asymptomatic, meaning that individuals typically do not notice any symptoms, which can make it challenging to detect without regular monitoring.

How is blood pressure maintained in the body?

Blood pressure is maintained by several factors including the contraction of the left ventricle, systemic vascular resistance, elasticity of the arterial walls, and blood volume. It is essentially the product of cardiac output and systemic vascular resistance.

What are baroreceptors and how do they regulate blood pressure?

Baroreceptors are pressure-sensitive neurons located in the aortic arch and carotid sinuses. They regulate blood pressure by sending signals to the adrenal medulla when blood pressure falls too low, causing the release of catecholamines and increasing sympathetic activity.

How does the renin-angiotensin-aldosterone system contribute to blood pressure regulation?

The renin-angiotensin-aldosterone system plays a significant role in blood pressure regulation. When blood pressure or blood flow to the kidneys falls, baroreceptors in the kidneys release renin, which is necessary for the production of angiotensin II, a potent vasoconstrictor that increases peripheral resistance and blood volume, ultimately leading to increased blood pressure.

What are alpha-1 blockers and how do they affect blood pressure?

Alpha-1 blockers, such as Doxazosin and Prazosin, work by blocking alpha-1 receptors on smooth muscle, leading to a decrease in systemic vascular resistance and, consequently, a decrease in blood pressure.

What is the role of beta blockers in treating hypertension?

Beta blockers, such as Atenolol and Metoprolol, selectively block beta-1 receptors on the heart, reducing cardiac output and thereby decreasing blood pressure. Non-selective beta blockers like Labetalol and Carvedilol can also block alpha-1 receptors, further decreasing vascular resistance.

How do centrally acting adrenergic drugs lower blood pressure?

Centrally acting adrenergic drugs, such as Clonidine and Methyldopa, work by blocking sympathetic activity within the brain. They stimulate presynaptic alpha-2 receptors, reducing catecholamine production and release, which leads to decreased systemic vascular resistance and cardiac output, and ultimately lowers blood pressure.

What are calcium channel blockers and how do they impact blood pressure?

Calcium channel blockers are divided into dihydropyridines and nondihydropyridines. Dihydropyridines selectively inhibit L-type calcium channels in vascular smooth muscle, reducing vascular resistance and blood pressure. Nonditihydropyridines block calcium channels in both vascular smooth muscle and cardiac cells, leading to reduced myocardial contractility, slower heart rate, and vasodilation, which also contributes to lowering blood pressure.

What are the different types of diuretics and how do they treat hypertension?

Diuretics used in hypertension treatment include loop diuretics, thiazide diuretics, and potassium-sparing diuretics. Loop diuretics like Furosemide reduce sodium chloride reabsorption, leading to significant diuresis and decreased blood pressure. Thiazide diuretics reduce sodium chloride reabsorption to a lesser extent and are thought to produce sustained antihypertensive effects through vasodilation. Potassium-sparing diuretics either interfere with sodium potassium exchange in the kidneys or block aldosterone actions, increasing diuresis and often used in combination with other diuretics to prevent potassium loss.

How do agents that work on the renin-angiotensin-aldosterone system reduce blood pressure?

Agents that work on the renin-angiotensin-aldosterone system reduce blood pressure by either inhibiting the production of angiotensin II or blocking its actions on the AT1 receptors. This leads to decreased systemic vascular resistance without significant changes in cardiac output and also improves renal blood flow, reducing the risk of renal injury.

What are some side effects associated with the use of dihydropyridines?

Side effects of dihydropyridines, which are related to systemic vasodilation, can include dizziness, headache, flushing, peripheral edema, and in some cases, gingival hyperplasia, or swelling of the gums.

What are the potential side effects of ACE inhibitors?

ACE inhibitors may cause dry cough and, in rare cases, angioedema, which can be life-threatening. These side effects are thought to be due to increased levels of bradykinin and substance P resulting from the inhibition of the angiotensin-converting enzyme.

What is unique about the mechanism of action of Fenoldopam in treating hypertension?

Fenoldopam is a selective dopamine-1 receptor agonist that produces generalized arterial vasodilation, leading to decreased peripheral resistance and lower blood pressure. It also inhibits tubular sodium reabsorption, resulting in natriuresis and diuresis. Due to its rapid onset and short duration of action, Fenoldopam is often used in hospitals for the short-term management of severe hypertension.

Outlines

00:00

💊 Introduction to Antihypertensive Pharmacology

The lecture begins with an introduction to the pharmacology of antihypertensive drugs, focusing on hypertension as a common disorder often without noticeable symptoms. It explains the basic physiology of blood pressure regulation, including the role of cardiac output, systemic vascular resistance, arterial wall elasticity, and blood volume. The importance of baroreceptors and the renin-angiotensin-aldosterone system in maintaining blood pressure is highlighted. The paragraph sets the stage for a deeper dive into various classes of antihypertensive agents and their mechanisms of action.

05:04

🛡️ Antihypertensive Agents and Their Mechanisms

This paragraph delves into the different classes of antihypertensive drugs, starting with alpha-1 blockers like Doxazosin and Prazosin, which reduce systemic vascular resistance. Selective and non-selective beta blockers such as Atenolol, Metoprolol, Labetalol, and Carvedilol are discussed for their effects on cardiac output and renin release. Centrally acting adrenergic drugs like Clonidine and Methyldopa are mentioned for their role in reducing sympathetic activity. Calcium channel blockers, divided into dihydropyridines and nondihydropyridines, are explained for their impact on vascular smooth muscle contraction and cardiac function. The summary underscores the variety of approaches to managing high blood pressure through pharmacological intervention.

10:06

💧 Diuretics and Their Impact on Blood Pressure

The role of diuretics in treating hypertension is explored, with a focus on three main classes: loop diuretics like Furosemide, which promote diuresis and reduce blood volume; thiazide diuretics like Hydrochlorothiazide, which cause initial volume reduction and long-term vasodilation; and potassium-sparing diuretics such as Triamterene and Spironolactone, which prevent potassium loss. The paragraph explains how these diuretics contribute to lowering blood pressure by affecting sodium and water balance in the body, with an emphasis on their unique mechanisms and the importance of potassium conservation.

🌀 The Renin-Angiotensin-Aldosterone System in Antihypertensive Therapy

This paragraph discusses the pharmacological targeting of the renin-angiotensin-aldosterone system to treat hypertension. It describes renin inhibitors like Aliskiren, ACE inhibitors such as Benazepril and Captopril, and angiotensin II receptor blockers (ARBs) like Candesartan and Losartan. The mechanisms by which these drugs reduce angiotensin II production or block its effects are detailed, highlighting their role in decreasing systemic vascular resistance and protecting the kidneys from injury. The potential side effects of these drugs, including hyperkalemia and the risk of cough or angioedema with ACE inhibitors, are also noted.

🚑 Other Antihypertensive Agents and Their Applications

The final paragraph covers additional antihypertensive agents that do not fit into the previously discussed classes. It mentions Bosentan, an antagonist of endothelin-1, used for pulmonary hypertension; Fenoldopam, a dopamine-1 receptor agonist for short-term severe hypertension management; and fast-acting agents like Sodium Nitroprusside and Nitroglycerin, which are sources of nitric oxide for emergency hypertension treatment. The paragraph also touches on direct-acting smooth muscle relaxants like Hydralazine and Minoxidil, which are often combined with other drugs to manage their side effects. The unique use of Minoxidil for hair growth is also highlighted, concluding the lecture with a broad view of the antihypertensive drug landscape.

Keywords

💡Hypertension

Hypertension, also known as high blood pressure, is a common medical condition characterized by persistently elevated arterial blood pressure. In the video, hypertension is the central theme, as the speaker discusses the pharmacology of antihypertensive drugs designed to treat this disorder. The script mentions that many people with hypertension may not exhibit noticeable symptoms, highlighting the importance of medical monitoring and treatment.

💡Blood Pressure Regulation

Blood pressure regulation is a physiological process that maintains the force of blood against artery walls. The video script delves into how blood pressure is regulated by various systems, including the baroreceptors, the renin-angiotensin-aldosterone system, and others. Understanding blood pressure regulation is crucial for grasping how antihypertensive drugs work to manage hypertension.

💡Baroreceptors

Baroreceptors are pressure-sensitive neurons located in the aortic arch and carotid sinuses that play a key role in blood pressure regulation. The script explains how these receptors respond to changes in blood pressure by signaling the adrenal medulla to release catecholamines, which in turn increase sympathetic activity and affect blood pressure through various mechanisms.

💡Renin-Angiotensin-Aldosterone System

The renin-angiotensin-aldosterone system is a hormone system that regulates blood pressure and fluid balance. The video describes how this system works, with baroreceptors in the kidneys releasing renin in response to low blood pressure, leading to the production of angiotensin II, a potent vasoconstrictor. This system is a target for several antihypertensive drugs discussed in the script.

💡Antihypertensive Agents

Antihypertensive agents are medications used to treat hypertension by lowering blood pressure. The video provides an overview of various classes of these drugs, such as alpha-1 blockers, beta blockers, and others, which work by interrupting different parts of the blood pressure regulating system. The script emphasizes the importance of these agents in managing high blood pressure.

💡Alpha-1 Blockers

Alpha-1 blockers, such as Doxazosin and Prazosin mentioned in the script, are a class of antihypertensive drugs that work by blocking alpha-1 receptors on smooth muscle, leading to a decrease in systemic vascular resistance and a subsequent drop in blood pressure. They are an example of how specific drug classes target different aspects of blood pressure regulation.

💡Beta Blockers

Beta blockers are another class of antihypertensive drugs that selectively block beta-1 receptors on the heart, reducing cardiac output and thus lowering blood pressure. The script also mentions non-selective beta blockers that can block alpha-1 receptors as well, providing a dual mechanism for blood pressure reduction.

💡Calcium Channel Blockers

Calcium channel blockers are a class of drugs that inhibit calcium channels, either selectively in vascular smooth muscle (dihydropyridines) or non-selectively including cardiac cells (nondihydropyridines). The script explains how these drugs reduce vascular resistance and cardiac output, leading to lowered blood pressure. They are an important class of antihypertensive agents with distinct mechanisms of action.

💡Diuretics

Diuretics are medications that increase urine production and are used to treat hypertension by reducing blood volume and cardiac output. The video script discusses three classes of diuretics: loop diuretics, thiazide diuretics, and potassium-sparing diuretics, each with different mechanisms of action and side effects.

💡Renin Inhibitors

Renin inhibitors are a class of antihypertensive drugs that target the renin enzyme, responsible for the production of angiotensin II. By inhibiting renin, these drugs decrease the production of angiotensin II, leading to reduced vasoconstriction and blood pressure. Aliskiren is an example of a renin inhibitor mentioned in the script.

💡Angiotensin II Receptor Blockers (ARBs)

Angiotensin II receptor blockers, or ARBs, are a class of drugs that block the AT1 receptors, preventing the vasoconstrictive effects of angiotensin II. The script lists several ARBs, such as Candesartan and Losartan, which reduce blood pressure by decreasing systemic vascular resistance without significantly affecting cardiac output.

Highlights

Hypertension is a common disorder often without noticeable symptoms.

Blood pressure is the force of blood against artery walls, influenced by cardiac output and systemic vascular resistance.

Baroreceptors in the aortic arch and carotid sinuses regulate arterial blood pressure through signals to the adrenal medulla.

Activation of beta-1 receptors increases heart rate and stroke volume, elevating blood pressure.

The renin-angiotensin-aldosterone system plays a key role in blood pressure regulation, with renin initiating the production of angiotensin II.

Angiotensin II is a potent vasoconstrictor that increases blood pressure by constricting systemic blood vessels and renal blood vessels.

Alpha-1 blockers like Doxazosin reduce blood pressure by blocking alpha-1 receptors and decreasing vascular resistance.

Selective beta blockers decrease cardiac output by blocking beta-1 receptors on the heart.

Non-selective beta blockers also block alpha-1 receptors, reducing both cardiac output and vascular resistance.

Centrally acting adrenergic drugs like Clonidine lower blood pressure by reducing sympathetic activity in the brain.

Calcium channel blockers are divided into dihydropyridines and nondihydropyridines, each affecting blood pressure differently.

Dihydropyridines reduce vascular resistance by inhibiting calcium channels in vascular smooth muscle.

Nondihydropyridines block calcium channels in cardiac cells, affecting heart rate and conduction, with potential antiarrhythmic properties.

Diuretics are categorized into loop, thiazide, and potassium-sparing diuretics, each impacting blood pressure and fluid balance differently.

Agents targeting the renin-angiotensin-aldosterone system reduce blood pressure by inhibiting angiotensin II production or its effects.

ACE inhibitors lower angiotensin II levels and may cause a dry cough due to increased bradykinin levels.

ARBs block angiotensin II receptors, reducing vascular resistance without affecting cardiac output.

Other antihypertensive agents like Bosentan and Fenoldopam have unique mechanisms for reducing blood pressure.

Direct acting smooth muscle relaxants like Hydralazine decrease peripheral resistance but may cause reflex tachycardia.

Minoxidil, used topically for hair growth, can also be an antihypertensive agent due to its vasodilatory effects.

Transcripts

in this lecture I'm going to talk about pharmacology of antihypertensive drugs

so let's get right into it hypertension or high blood pressure is a

quite common disorder affecting many people who typically don't even notice

any symptoms now in order to gain a better understanding of pharmacology of

antihypertensive agents first we need to review a basic physiology of blood

pressure regulation so when we talk about blood pressure we are generally

referring to the force or tension of blood pressing against the artery walls

now this pressure in the arteries is maintained by among other things

contraction of the left ventricle systemic vascular resistance elasticity

of the arterial walls as well blood volume in other words blood pressure is

simply a product of cardiac output and systemic vascular resistance there are a

couple of major systems involved in blood pressure regulation first arterial

blood pressure is regulated by pressure sensitive neurons called baroreceptors

located in the aortic arch and carotid sinuses so for example if blood pressure

falls too low those baroreceptors can send signals to the adrenal medulla

causing release of catecholamines and thus increase in sympathetic activity through

activation of alpha and beta receptors so activation of beta-1 receptors causes

increase in heart rate and stroke volume and thus increased cardiac output which

leads to increase in blood pressure on the other hand activation of alpha-1

receptors on smooth muscle causes vasoconstriction and thus increase in

vascular resistance which again leads to increase in blood pressure now another

major system involved in blood pressure regulation is the

renin-angiotensin-aldosterone system so we also have baroreceptors in the

kidneys that respond to fall in blood pressure or reduction of blood flow by

releasing enzyme called renin additionally renin secretion is also

stimulated by sympathetic activation of beta-1 receptors

in the kidneys now renin is necessary for the production of angiotensin II

angiotensin II is a very potent vasoconstrictor which constricts systemic

blood vessels thus increasing peripheral resistance angiotensin II also

constricts renal blood vessels and stimulates aldosterone secretion which

leads to sodium and water retention thereby increased blood volume cardiac

output and ultimately increased blood pressure now let's switch gears and

let's talk about antihypertensive agents so there are several major

classes of antihypertensive drugs which work by interrupting different parts of

this blood pressure regulating system first we have alpha-1 blockers such as

Doxazosin and Prazosin which block alpha-1 receptors on the smooth muscle

thus causing decrease in systemic vascular resistance and ultimately

decrease in blood pressure next we have selective beta blockers such as Atenolol

and Metoprolol which selectively block beta-1 receptors on the heart thus

causing decrease in cardiac output and thereby decrease in blood pressure as

you may remember we also have non-selective beta blockers such as

Labetalol and Carvedilol that can additionally block alpha-1 receptors and

thus simultaneously decrease vascular resistance furthermore beta blockers can

inhibit beta-1 receptors present on the kidneys and thus suppress release of

renin formation of angiotensin II and secretion of aldosterone so these

effects result in decrease in systemic vascular resistance and again fall in

blood pressure to learn more about alpha and beta blockers make sure you check

out my video about adrenergic antagonists now the next major class of

antihypertensive agents are centrally acting adrenergic drugs which work by

blocking sympathetic activity within the brain example of drugs that belong to

this class are Clonidine and Methyldopa now Clonidine selectively stimulates

presynaptic alpha-2 receptors thus providing negative feedback to reduce

catecholamine production and release this leads to decrease

in systemic vascular resistance and cardiac output and ultimately decreased

blood pressure Methyldopa on the other hand also lowers blood pressure through the

same mechanism however unlike Clonidine it is not an

agonist itself so first it must be converted to its active metabolite

called methylnorepinephrine now let's move on to another major class of

antihypertensive agents that is calcium channel blockers so calcium channel

blockers are divided into two main subclasses dihydropyridines and

nondihydropyridines now dihydropyridines selectively inhibit L-type calcium

channels in the vascular smooth muscle under normal conditions when calcium

enters the smooth muscle cell it causes it to contract which leads to increased

vascular resistance and thus increase in blood pressure so when dihydropyridine drug

blocks the entry of calcium into the vascular smooth muscle cell the

contraction is inhibited which leads to decreased resistance to blood flow and

thus lowering of blood pressure example of drugs that belong to this group are

Amlodipine Felodipine Nicardipine and Nifedipine when it comes to side

effects of dihydropyridines they're related to systemic vasodilation so you

can expect dizziness headache flushing and peripheral edema another side effect

that may occur with this class is swelling of gums also known as gingival

hyperplasia now let's move on to nondihydropyridines which are non selective

inhibitors of L-type calcium channels in other words they are not only capable of

blocking calcium channels on vascular smooth muscle but also calcium channels

on cardiac cells such as those of SA node and AV node which leads to reduced

myocardial contractility slower heart rate and slower conduction that's why these

agents exhibit significant antiarrhythmic properties for more

details make sure you check out my video about antiarrhythmic drugs

now it's important to remember that even though decreased heart contractions

typically result in decreased cardiac output

nondihydropyridines do not significantly decrease cardiac output

most likely because of the reflex tachycardia that occurs as a result of

vasodilation currently there are only two drugs that belong to this group

namely Diltiazem and Verapamil now when it comes to side-effects nondihydropyridines

can cause excessive bradycardia and cardiac conduction abnormalities

additionally Verapamil which happens to be the least selective calcium channel

blocker can exert significant inhibition of calcium channels in the smooth muscle

that lines the GI tract which can lead to constipation

now the next major class of antihypertensive agents are diuretics there

are three major classes of diuretics that are used in the treatment of

hypertension first we have loop diuretics such as Furosemide which

work by reducing reabsorption of sodium chloride in the kidneys leading to

significant diuresis with less volume in the vascular space less blood returns to

the heart so cardiac output decreases this in turn leads to decrease in blood

pressure particularly in patients with volume-based hypertension and chronic

kidney disease secondly we have thiazide diuretics such as Hydrochlorothiazide

which also reduce reabsorption of sodium chloride in the kidneys but to a much

smaller degree than loop diuretics this leads to initial decrease in

intravascular volume decrease in cardiac output and ultimately lower blood

pressure however the long term effects on blood volume are minimal and

sustained antihypertensive effects are thought to be produced by thiazide induced

vasodilation lastly we have potassium-sparing diuretics such as Triamterene

and Spironolactone which increase diuresis by either interfering with the

sodium potassium exchange in the kidneys or by blocking the actions of

aldosterone potassium-sparing diuretics are often used in combination

with loop and thiazide diuretics to reduce loss of potassium that can occur with

the use of these drugs for more details make

sure you check out my video about diuretics now let's move on to another

group of antihypertensive agents that is agents that work on the

renin-angiotensin-aldosterone system so here we have three pharmacological

targets that can be used to reduce the activity of angiotensin II which is

ultimately responsible for causing blood pressure to increase first we have renin

the enzyme responsible for conversion of angiotensinogen to precursor of

angiotensin II that is angiotensin I so renin is the target of renin inhibitors

which selectively inhibit this enzyme thus decreasing production of

angiotensin II the example of drug that belongs to this class is Aliskiren

secondly we have angiotensin-converting enzyme that is responsible

for conversion of angiotensin I to angiotensin II this enzyme is the target

of ACE inhibitors so just like inhibition of renin inhibition of

angiotensin-converting enzyme also leads to decreased production of angiotensin II

however what makes ACE inhibitors different is that in addition to

lowering angiotensin II levels they can also elevate bradykinin levels

bradykinin is a peptide that causes blood vessels to dilate by stimulating

the release of nitric oxide and prostacyclin

however normally angiotensin-converting enzyme inactives bradykinin so it's

inhibition leads to bradykinin induced vasodilation the example of drugs

that belong to this class are Benazepril Captopril Enalapril

Lisinopril Quinapril and Ramipril finally we have

angiotensin II receptors type 1 or AT1 receptors for short so binding

of angiotensin II to these receptors is actually responsible for most of the

effects of angiotensin II including vasoconstriction and stimulation of

aldosterone release these receptors are the target of angiotensin II receptor

blockers or ARBs for short the example of drugs that

belong to this class are Candesartan Irbesartan Losartan Olmesartan and

Valsartan so in summary the agents that work on

this renin-angiotensin-aldosterone system either block the production of

angiotensin II or block its actions on the AT1 receptors this in turn leads to

decreased systemic vascular resistance but without significant changes in

cardiac output additionally these agents reduce the effects of angiotensin II on

renal hemodynamics specifically angiotensin II constricts the efferent

arteriole thereby generating back pressure in the glomerulus which can

lead to injury so by reducing activity of angiotensin II these agents also

improve renal blood flow and thereby reduce the risk of renal injury now when

it comes to side effects because these agents suppress aldosterone release

their use can contribute to development of hyperkalemia furthermore

ACE inhibitors in particular may cause dry cough or in rare cases angioedema

which can be life-threatening this is thought to be due to increased

levels of bradykinin and substance P now before we end this lecture I wanted to

briefly discuss few other antihypertensive agents that do not fall

into any of the classes that we covered thus far so first we have Bosentan

which is a competitive antagonist of a potent vasoconstrictor called endothelin-1

which acts on the endothelin-A and endothelin-B receptors located

on pulmonary vascular cells by blocking the action of endothelin-1 on

these receptors Bosentan leads to vasodilation which decreases pulmonary

vascular resistance for that reason Bosentan is often a drug of choice for

treatment of pulmonary hypertension next we have Fenoldopam which is a selective

dopamine-1 receptor agonist the dopamine-1 receptors are located on the

smooth muscle cells in the peripheral vasculature

as well as the renal coronary cerebral and mesenteric arteries by stimulating

dopamine-1 receptors Fenoldopam produces generalized arterial vasodilation

which leads to decreased peripheral resistance and thus lower blood pressure

additionally Fenoldopam inhibits tubular sodium reabsorption which

results in natriuresis and diuresis due to its rapid onset of action and

short duration of action Fenoldopam is often used in the

hospitals for short-term management of severe hypertension another fast-acting

agents that are also used for hypertensive emergency are

Sodium Nitroprusside and Nitroglycerin which simply serve as a source of nitric oxide

a potent peripheral vasodilator lastly we have direct acting smooth muscle

relaxants namely Hydralazine with mechanism of action that has not been

entirely determined yet and Minoxidil which works by stimulating opening of

ATP-activated potassium channels in the smooth muscle which leads to membrane

stabilization making vasoconstriction less likely while these agents

significantly decrease peripheral resistance they also produce significant

compensatory reflex tachycardia and renin release for that reason these

drugs are typically administered in combination with a diuretic and a beta

blocker on the flip side topical application of Minoxidil promotes hair

growth which is why this drug is used more often for treatment of baldness

rather than hypertension and with that I wanted to thank you for watching I hope

you enjoyed this video and as always stay tuned for more