Cardiovascular pharmacology Flashcards
Choose the single best answer(5p)
6:1 What is true about digoxin that can be used to treat heart failure?
a)It dilates arteries by relaxing smooth muscle cells
b)It stimulates the Na+/K+ ATPase of the hearts muscle cells
c)It ́s mechanisms of action leads to more calcium inside the hearts muscle cells
d)It blocks the effect of adrenaline
Digoxin increases the force of contraction in the heart by increasing the amount of calcium available to the myocardial cells. This increased calcium availability leads to an increased number of cross-bridges formed between actin and myosin, which increases the strength of contraction. Additionally, digoxin increases the sensitivity of the myocardial cells to calcium, further increasing the force of contraction. Finally, digoxin also increases the rate at which calcium is released from the sarcoplasmic reticulum, which further increases the amount of calcium available for contraction. All these effects combine to increase the force of contraction in the heart.
So C is the best answer
Choose the single best answer:
6:2 Enalapril is used to treat hypertension. Which statement below can be related to enalapril’s effects?
a)Blockade of the angiotensin type 1 receptor
b)Reduction the amount of angiotensin 1
c)Reduction in arterial contraction
d)Increased absorption of sodium in the kidney
ACE-inhibitors
angiotensin converting enzyme: it converts angiotensin I to angiotensin II, which is important in the regulation of blood pressure.
In this case, if the enzyme is inhibited (Enalapril is an example of an inhibitor that could be used), less conversion of angiotensin I to angiotensin II will be obtained → blood pressure is reduced.
Enalapril is an ACE inhibitor, which stands for angiotensin-converting enzyme inhibitor. It works by blocking the action of an enzyme called angiotensin-converting enzyme (ACE). This enzyme is responsible for converting a hormone called angiotensin I into a more potent form called angiotensin II. Angiotensin II causes blood vessels to constrict, which increases blood pressure. By blocking the action of ACE, enalapril prevents the formation of angiotensin II and thus reduces blood pressure. It also helps to relax and widen the blood vessels, allowing for increased blood flow through the arteries. This increased blood flow can help reduce the risk of heart attack and stroke.
The best answer is therefore c
Choose the single best answer:
6:3 What is true about nitrates that are used in coronary artery disease?
a)They will stimulate the production of nitric oxide
b)They will contract arteries
c)They will slow down the heart rate
d)They will improve blood supply to the heart
Nitrates are medications used to treat coronary artery disease, which is a condition in which the arteries that supply blood to the heart become narrowed or blocked.
Nitrates can increase blood flow to the heart. Nitrates are vasodilators, meaning they relax and widen the blood vessels, allowing more blood to flow through them.
The best answer is d
Choose the single best answer:
6:4 Furosemide can be used to treat cardiovascular disease. What is true about its effect?
a)They block water channels in the kidney
b)They reduce urine production
c)They block the re-uptake of Na+ in the kidney
d)They block cyclooxygenases in the kidney
Furosemide is a diuretic medication used to treat cardiovascular disease. It works by increasing the amount of salt and water that the kidneys remove from the blood, which helps to reduce the amount of fluid in the body. This helps to reduce blood pressure, which can help to prevent heart failure, stroke, and other cardiovascular problems.
Furosemide is a loop diuretic, which means it works by inhibiting the reabsorption of sodium and chloride ions in the ascending loop of Henle in the kidneys. This causes an increased excretion of water, electrolytes, and other substances from the body.
The best answer is therefore c
Choose the single best answer:
6:5 Which of the following drug actions can lead to reduced contraction of arteries and reduced arterial pressure?
a)activation of α1-adrenoceptors
b)blockade of calcium channels
c)activation of aldosterone receptors
d)activation of calcium channels
Blocking calcium channels in smooth muscle tissue causes the muscle to relax. This is because calcium is necessary for the contraction of smooth muscle cells. When calcium channels are blocked, the amount of calcium entering the cell is reduced, which prevents the muscle from contracting. This can be beneficial in treating conditions such as hypertension, where relaxation of the smooth muscle cells in the walls of blood vessels can help reduce blood pressure.
The best answer is therefore b
Which receptors does “betablockers” act on in the heart (for full point the correct receptor nomenclature needs to be used)?
Which effects does “betablockers” have on the function of the heart (for full point the cell types and related function must be given)? (3p)
The effects via the sympathetic branch of the autonomic nervous system on the heart is mediated via beta 1 adrenoceptors and it will increase the frequency of the heart by effects on autorhythmic cells, its gonna increase the force by effects on cardiomyocytes
Betablockers act on beta-adrenergic receptors in the heart. These receptors are located on the surface of cardiac muscle cells and are responsible for mediating the effects of the hormones epinephrine and norepinephrine. When these hormones bind to the beta-adrenergic receptors, they cause an increase in heart rate, contractility, and conduction velocity. Betablockers work by blocking these receptors, thus preventing the hormones from binding and reducing their effects on the heart. This can help to reduce blood pressure, slow down a rapid heart rate, and reduce the risk of arrhythmias.
The beta-adrenergic receptors in the heart are divided into two subtypes: β1 and β2.
The β1 receptors are located mainly in the sinoatrial node, atrioventricular node, and ventricular myocardium. They are responsible for increasing heart rate, contractility, and conduction velocity.
The β2 receptors are located mainly in the atria and coronary arteries. They are responsible for vasodilation of the coronary arteries, which increases blood flow to the heart muscle.
In the heart, beta-adrenergic receptors are primarily located on the sinoatrial node (SA node), atrioventricular node (AV node), and ventricular myocytes. Beta-adrenergic receptors are also found in the coronary arteries, where they regulate blood flow to the heart muscle.
Nodal cells in the heart have an action potential that differ in shape from the action potential of ventricular cardiomyocytes. Describe with your own words what is unique with the nodal action potential. Also, describe mechanistically what underlies the ability of nodal cells to fire spontaneously and act as “pacemakers” of the heart.
Nodal cells do not have a stable resting membrane potential but instead exhibit a slow depolarization due to the influx of sodium (Na+) and calcium (Ca2+) ions through specialized ion channels called funny channels (If). This phase gives the nodal cells their automaticity, meaning they can generate an action potential spontaneously without external stimulation.
Once the membrane potential reaches a threshold level, voltage-gated calcium channels (Ca2+) open, leading to a rapid depolarization of the cell membrane. This phase is responsible for the initiation of the action potential.
After reaching its peak, the membrane potential repolarizes slowly due to the opening of voltage-gated potassium (K+) channels and closing of the voltage-gated calcium channels. This phase prepares the cell for the next action potential.
Mechanistically, the unique ability of nodal cells to fire spontaneously and act as pacemakers is due to the presence of specialized ion channels and transporters. The main contributors to the spontaneous depolarization are the funny channels (If) that allow a slow influx of sodium (Na+) and calcium (Ca2+) ions during phase 4. The Na+/K+ ATPase pump maintains the ion concentration gradient necessary for the function of the cardiac cells. The rate of funny channel activation determines the rate of depolarization, which determines the heart rate.
In addition to the funny channels, nodal cells also have a variety of other ion channels that contribute to the action potential, such as voltage-gated calcium channels (Ca2+) and potassium channels (K+). The interplay between these channels determines the shape and duration of the action potential.
Upon a routine medical examination of a patient, which included taking an electrocardiogram, a prolonged QT interval was observed. You suspect that the prolonged QT interval is an adverse effect of one of the medical drugs the patient is taking. Which cardiac ion channel may the drug be acting on? Motivate your choice by explaining the role of this ion channel in the heart.
The drug in question may be acting on the Kv channels, as these channels are responsible for the repolarization of the ventricles during the QT interval. When a drug blocks the Kv11.1 channel, it impairs the repolarization of the ventricles and prolongs the QT interval.
You are a cardiomyocyte who wants to spontaneously generate action potentials. Describe how you can make this possible. Your description should include information about what ion channel(s) to use and what ions to utilize.
Nodal cells do not have a stable resting membrane potential but instead exhibit a slow depolarization due to the influx of sodium (Na+) and calcium (Ca2+) ions through specialized ion channels called funny channels (If). This phase gives the nodal cells their automaticity, meaning they can generate an action potential spontaneously without external stimulation.
Once the membrane potential reaches a threshold level, voltage-gated calcium channels (Ca2+) open, leading to a rapid depolarization of the cell membrane. This phase is responsible for the initiation of the action potential.
After reaching its peak, the membrane potential repolarizes slowly due to the opening of voltage-gated potassium (K+) channels and closing of the voltage-gated calcium channels. This phase prepares the cell for the next action potential.
Mechanistically, the unique ability of nodal cells to fire spontaneously and act as pacemakers is due to the presence of specialized ion channels and transporters. The main contributors to the spontaneous depolarization are the funny channels (If) that allow a slow influx of sodium (Na+) and calcium (Ca2+) ions during phase 4. The Na+/K+ ATPase pump maintains the ion concentration gradient necessary for the function of the cardiac cells. The rate of funny channel activation determines the rate of depolarization, which determines the heart rate.
In addition to the funny channels, nodal cells also have a variety of other ion channels that contribute to the action potential, such as voltage-gated calcium channels (Ca2+) and potassium channels (K+). The interplay between these channels determines the shape and duration of the action potential.
You are developing an experimental model of a cardiomyocyte with decreased action potential duration. Describe two types of ion channels you could target to achieve this and explain how channel activity would need to be altered. Motivate your choice by explaining the role of these ion channels in the cardiac action potential.
One type of ion channel that could be targeted to decrease the action potential duration of a cardiomyocyte is the potassium ion channel. Specifically, the rapid delayed rectifier potassium current (Ikr) is a crucial player in repolarizing the cardiac action potential. Therefore, targeting Ikr channels could result in a shorter action potential duration. In order to achieve this, the activity of Ikr channels would need to be reduced. This can be done using drugs such as dofetilide, which specifically blocks the activity of Ikr channels.
Another type of ion channel that could be targeted is the L-type calcium ion channel. During the plateau phase of the cardiac action potential, the influx of calcium ions through L-type calcium channels helps to maintain depolarization. Therefore, inhibiting the activity of these channels can lead to a shorter action potential duration. This can be achieved using drugs such as verapamil, which specifically block L-type calcium channels.
Both of these ion channels play crucial roles in the cardiac action potential. Ikr channels are responsible for the repolarization phase of the action potential, while L-type calcium channels are responsible for the depolarization phase.
When is nitroglycerin used clinically?
How is the drug administered? Motivate and explain why the drug is administrated the way you answered.
Nitroglycerin is a medication that is primarily used clinically to treat and manage chest pain (angina) and heart failure. It works by relaxing the smooth muscles in blood vessels, which leads to dilation of the blood vessels, increased blood flow, and reduced workload on the heart.
The most common and preferred route of administration for acute angina is sublingual. Nitroglycerin tablets are placed under the tongue, where they dissolve and are rapidly absorbed into the bloodstream. This route of administration provides quick relief of angina symptoms, typically within 1-2 minutes. It’s so it can have a fast acting effect since it’s a acute state that needs to be treated as quickly as possible.
Your colleague is fascinated by the sinoatrial node and asks for your advice on what type of pharmacological drug to use to reduce the heart rate (i.e. frequency of firing). Explain your preferred type of drug to achieve such an effect. Motivate your choice by explaining to your colleague the mechanism of action of your preferred type of drug in the sinoatrial node.
Beta-blockers work by blocking the beta-adrenergic receptors located in the heart and other tissues. These receptors are responsible for receiving signals from the sympathetic nervous system, which can increase heart rate and contractility. Specifacally Beta blockers -1 since it’s located on for example the SA node.
Some anti-arrhythmic drugs primarily affect cardiomyocytes that fire with abnormally fast heart rate. Describe the mechanism underlying this behavior of drugs.
Class IV anti-arrhythmic drugs, such as verapamil and diltiazem, block the calcium channels in the cardiomyocytes, reducing the influx of calcium ions into the cell. This action slows down the depolarization of the cell and the firing of the action potential, thereby decreasing the heart rate.
Which receptors does “betablockers” act on in the heart (for full point the correct
receptor nomenclature needs to be used)? Which effects does “betablockers” have
on the function of the heart (for full point the cell types and related function must
be given)?
The effects via the sympathetic branch of the autonomic nervous system on the heart is mediated via beta 1 adrenoceptors and it will increase the frequency of the heart by effects on autorhythmic cells, its gonna increase the force by effects on cardiomyocytes
Betablockers act on beta-adrenergic receptors in the heart. These receptors are located on the surface of cardiac muscle cells and are responsible for mediating the effects of the hormones epinephrine and norepinephrine. When these hormones bind to the beta-adrenergic receptors, they cause an increase in heart rate, contractility, and conduction velocity. Betablockers work by blocking these receptors, thus preventing the hormones from binding and reducing their effects on the heart. This can help to reduce blood pressure, slow down a rapid heart rate, and reduce the risk of arrhythmias.
The beta-adrenergic receptors in the heart are divided into two subtypes: β1 and β2.
The β1 receptors are located mainly in the sinoatrial node, atrioventricular node, and ventricular myocardium. They are responsible for increasing heart rate, contractility, and conduction velocity.
The β2 receptors are located mainly in the atria and coronary arteries. They are responsible for vasodilation of the coronary arteries, which increases blood flow to the heart muscle.
In the heart, beta-adrenergic receptors are primarily located on the sinoatrial node (SA node), atrioventricular node (AV node), and ventricular myocytes. Beta-adrenergic receptors are also found in the coronary arteries, where they regulate blood flow to the heart muscle.
Adrenergic and cholinergic signaling are important in the autonomic nervous system.
Explain, based on the structure of the autonomic nervous system, which division (or
divisions) of the autonomic nervous system that can be activated by a nicotinic agonist.
Nicotinic acetylcholine receptors are ionotropic receptors found on both sympathetic and parasympathetic ganglia, as well as in the neuromuscular junction. Therefore, a nicotinic agonist can activate both the sympathetic and parasympathetic divisions of the autonomic nervous system, as well as skeletal muscle.
When a nicotinic agonist binds to a nicotinic acetylcholine receptor in a ganglion, it leads to depolarization and subsequent release of neurotransmitters from the postganglionic neuron, which then act on target organs or tissues. In the sympathetic nervous system, this can result in increased heart rate, dilation of bronchioles, and increased blood pressure, among other effects. In the parasympathetic nervous system, nicotinic agonists can lead to decreased heart rate, constriction of bronchioles, and increased gastrointestinal motility, among other effects.
