Alpha and Beta Blockers Pharmacology

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Questions and Answers

What is the primary amino acid from which norepinephrine is made?

  • Cysteine
  • Phenylalanine
  • Tyrosine (correct)
  • Tryptophan

Which receptor type is associated with an increase in blood pressure due to smooth muscle contraction?

  • Alpha-2
  • Alpha-1 (correct)
  • Beta-1
  • Beta-2

Which receptor type causes vasodilation, bronchodilation, and glycogenolysis?

  • Alpha-2
  • Alpha-1
  • Beta-2 (correct)
  • Beta-1

What type of protein is associated with beta-1 receptors?

<p>Gs protein (A)</p> Signup and view all the answers

What happens when alpha-2 receptors are activated?

<p>Inhibition of norepinephrine release (C)</p> Signup and view all the answers

Which neurotransmitter preferentially binds to beta receptors?

<p>Epinephrine (B)</p> Signup and view all the answers

What causes the release of norepinephrine via exocytosis?

<p>Increase in intracellular calcium levels (D)</p> Signup and view all the answers

How is norepinephrine metabolized into an inactive metabolite?

<p>By catechol methyl transferase (B)</p> Signup and view all the answers

Which protein is associated with alpha-1 receptors?

<p>Gq protein (A)</p> Signup and view all the answers

What happens when Beta-2 receptors are activated?

<p>Vasodilation (B)</p> Signup and view all the answers

What stimulates voltage-gated calcium channels leading to the release of norepinephrine?

<p>Action potential along the neuron (C)</p> Signup and view all the answers

Which receptor type is associated with a decrease in sympathetic tone?

<p>Alpha-2 (B)</p> Signup and view all the answers

What is the primary effect of alpha blockers on the internal urethral sphincter?

<p>Relaxation (B)</p> Signup and view all the answers

Which receptors do alpha-2 receptors inhibit norepinephrine release from?

<p>Juxtaglomerular cells (B)</p> Signup and view all the answers

What physiological effect do beta blockers have on renin release from the juxtaglomerular cells?

<p>Inhibit (A)</p> Signup and view all the answers

What is the primary effect of beta blockers on beta-1 receptors in the heart?

<p>Decrease heart rate (A)</p> Signup and view all the answers

What potential adverse effect can result from inhibiting alpha-1 receptors with alpha blockers?

<p>Orthostasis (A)</p> Signup and view all the answers

Which receptors do beta blockers stimulate contraction and urination through?

<p>Beta-3 receptors (A)</p> Signup and view all the answers

What is the primary effect of alpha blockers on pupil constriction?

<p>Dilation (C)</p> Signup and view all the answers

Which physiological effect do beta blockers have on smooth muscle relaxation in the bronchioles?

<p>Inhibition (D)</p> Signup and view all the answers

What is the primary effect of beta-3 blocking drugs on lipolysis?

<p>Inhibit (B)</p> Signup and view all the answers

What is the main purpose of using beta-1 blockers in portal hypertension?

<p>Reduce cardiac output (A)</p> Signup and view all the answers

What potential adverse effect can result from using beta-1 blockers in patients with decompensated heart failure or super bradycardia?

<p>Bradycardia (D)</p> Signup and view all the answers

What type of urinary disorder can alpha-1 blockers be beneficial for?

<p>Incontinence due to an enlarged prostate (A)</p> Signup and view all the answers

Flashcards

Norepinephrine

Neurotransmitter released from adrenergic neurons, made from tyrosine, a specific amino acid. It binds to various receptors, influencing different physiological effects.

Tyrosine Transporter

A co-transporter in nerve terminals responsible for taking up tyrosine, the precursor molecule for norepinephrine.

Dopamine

Substance produced from tyrosine in nerve terminals, converted into norepinephrine within vesicles. It acts as a neurotransmitter and plays a role in regulating various bodily functions.

Vesicles

Small membrane-bound sacs containing norepinephrine within nerve terminals. They store and release norepinephrine upon stimulation.

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Voltage-Gated Calcium Channel

A protein channel in the neuron's membrane that opens in response to an action potential. It allows calcium ions to flow into the cell, triggering the release of neurotransmitters, such as norepinephrine.

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Exocytosis

Process by which vesicles containing neurotransmitters fuse with the cell membrane and release their contents into the synaptic space.

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Alpha Receptor

A type of receptor that binds to norepinephrine, located on various cells and tissues. It is involved in regulating various physiological processes, including blood pressure, heart rate, and smooth muscle contraction.

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Alpha-1 Receptor

A subtype of alpha receptor that couples to the Gq protein and increases intracellular calcium levels. It is found on smooth muscle cells of blood vessels and other tissues, leading to vasoconstriction and increased blood pressure.

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Alpha-2 Receptor

A subtype of alpha receptor that couples to the Gi protein and decreases intracellular cyclic AMP levels. It is found on presynaptic neurons, inhibiting norepinephrine release and decreasing sympathetic tone.

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Beta Receptor

A type of receptor that binds to norepinephrine, located on various cells and tissues. It is involved in regulating various physiological processes, including heart rate, contractility, and smooth muscle relaxation.

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Beta-1 Receptor

A subtype of beta receptor that couples to the Gs protein and increases intracellular cyclic AMP levels. It is found on the heart, causing increased heart rate, contractility, and secretion.

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Beta-2 Receptor

A subtype of beta receptor that couples to the Gs protein and increases intracellular cyclic AMP levels. It is found on various tissues, causing vasodilation, bronchodilation, and glycogenolysis in the liver.

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Epinephrine

A catecholamine like norepinephrine released from the adrenal medulla. It preferentially binds to beta receptors, particularly beta-2 receptors, causing various physiological effects.

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Catechol Methyl Transferase (COMT)

An enzyme that converts norepinephrine into an inactive metabolite. This process helps terminate the action of norepinephrine.

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Alpha Blockers

Drugs that block the effects of norepinephrine by binding to alpha receptors. They are used to treat conditions like hypertension and urinary retention caused by benign prostatic hyperplasia (BPH).

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Beta Blockers

Drugs that block the effects of norepinephrine and epinephrine by binding to beta receptors. They are used to treat conditions like high blood pressure, arrhythmias, and angina.

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Orthostasis

A potential adverse effect of alpha blockers, characterized by a sudden drop in blood pressure upon standing. It occurs because alpha blockers reduce venous return to the heart, decreasing blood pressure.

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Intraoperative Floppy Iris Syndrome (IFIS)

A condition where the iris, a colored part of the eye, becomes floppy during surgery. It is caused by alpha blockers, which constrict the pupil, affecting the iris muscles.

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Urological Benefit

A specific effect of using alpha blockers, particularly alpha-1 blockers, to treat urinary retention caused by benign prostatic hyperplasia (BPH). It works by relaxing the muscles in the bladder neck, making urination easier.

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Alpha-1 Blockers

Drugs that block the effects of alpha-1 receptors, causing relaxation of smooth muscle in blood vessels, sphincters, and the pupil. They are used to treat conditions like hypertension, BPH, and Raynaud's phenomenon.

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Beta-1 Blockers

Drugs that block the effects of beta-1 receptors, causing a decrease in heart rate and contractility. They are used to treat conditions like high blood pressure, angina, and arrhythmias.

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Bradycardia

A potential adverse effect of beta-1 blockers, characterized by a slow heart rate. It can be more pronounced in individuals with pre-existing heart problems or taking other medications that slow the heart rate.

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Study Notes

  • The text is about discussing adrenergic antagonists, specifically alpha and beta blockers.
  • Adrenergic neurons release neuroepinephrine, which is made from tyrosine, a specific amino acid.
  • Tyrosine is taken up into nerve terminals via co-transporter and converted into dopamine, which is then converted into noroepinephrine within the vesicles.
  • Norepinephrine is released via exocytosis when an action potential runs down the neuron, stimulating voltage-gated calcium channels.
  • Norepinephrine can bind to various receptors: alpha-1, alpha-2, beta-1, beta-2, and beta-3.
  • Alpha-1 receptors (Gq protein) increase intracellular calcium levels, causing smooth muscle contraction and increase in blood pressure.
  • Alpha-2 receptors (Gi protein) decrease intracellular cyclic AMP levels, inhibiting norepinephrine release and decreasing sympathetic tone.
  • Beta-1 receptors (Gs protein) increase intracellular cyclic AMP levels, causing increased heart rate, contractility, and secretion.
  • Beta-2 receptors (Gs protein) cause vasodilation, bronchodilation, and glycogenolysis in the liver.
  • Epinephrine, a catecholamine like norepinephrine, preferentially binds to beta receptors and is released from the adrenal medulla.
  • Norepinephrine can be metabolized by catechol methyl transferase into an inactive metabolite, or taken back up into the synaptic vesicle for recycling.
  • Alpha blockers inhibit the effects of norepinephrine at alpha receptors, decreasing systemic vascular resistance and blood pressure.
  • Beta blockers inhibit the effects of norepinephrine and epinephrine at beta receptors, opposing the increase in heart rate, contractility, and secretion.
  • Alpha blockers may inhibit contraction of the internal urethral sphincter, allowing for urination.
  • Alpha blockers can cause pupil constriction, leading to intraoperative floppy iris syndrome.
  • Alpha-2 receptors inhibit norepinephrine release, decreasing sympathetic tone.
  • Alpha-2 receptors in pancreatic beta cells increase insulin production and release, lowering blood glucose levels.
  • Beta blockers inhibit beta-1 receptors in the heart, decreasing contractility and heart rate.
  • Beta blockers inhibit renin release from the juxtaglomerular cells, decreasing the activity of the renin-angiotensin-aldosterone system and blood pressure.
  • Beta-2 receptors cause vasodilation and bronchodilation, but beta blockers inhibit these effects, potentially increasing resistance and blood pressure.
  • Beta blockers inhibit smooth muscle relaxation in the bronchioles, causing bronchoconstriction.
  • Beta blockers inhibit glycogenolysis and gluconeogenesis in the liver, potentially causing hypoglycemia.
  • Beta-3 receptors cause smooth muscle relaxation in the bladder, but beta blockers stimulate contraction and urination.
  • Beta blockers have non-selective effects on beta receptors, potentially causing lipolysis and free fatty acid release.- Epinephrine and norepinephrine bind to receptors, causing various physiological effects.
  • Alpha receptors oppose the actions of epinephrine and norepinephrine.
  • Alpha blockers prevent epinephrine and norepinephrine from binding to alpha receptors, inhibiting their effects.
  • Alpha blockers are more selective for alpha-1 receptors and have less affinity for alpha-2 receptors.
  • Beta-3 blocking drugs inhibit lipolysis and can increase triglycerides in the blood, potentially leading to both beneficial and adverse effects.
  • Alpha blockers are used to treat conditions such as high blood pressure, angina, and certain heart rhythm disorders.
  • Adverse effects of alpha blockers can include hypotension, dizziness, and bronchoconstriction.
  • Examples of alpha blockers include phentolamine, phenylephrine, and phenylephrine hydrochloride.- The text discusses various types of drugs called alpha and beta blockers, specifically alpha-1 blockers and beta-1 blockers
  • Alpha-1 blockers work by inhibiting the effects of alpha-1 receptors on blood vessels, sphincters, and the pupil
  • Inhibiting alpha-1 receptors can cause a decrease in venous return, leading to orthostasis as a potential adverse effect
  • Alpha-1 blockers can also decrease systemic vascular resistance, making them useful for treating hypertension
  • They can also be beneficial for patients with urinary incontinence caused by an enlarged prostate
  • Beta-1 blockers work by inhibiting the effects of beta-1 receptors on the heart, causing a decrease in heart rate and contractility
  • They can be useful in situations where there is an excessive production of adrenaline or thyroid hormones, as they can block the increased sensitivity of beta-1 receptors
  • Beta-1 blockers can also be used prophylactically in portal hypertension to reduce the risk of varices and upper GI bleeds
  • They can also be used to reduce cerebral blood flow and inhibit pain receptors, making them useful in migraine prophylaxis
  • Beta-1 blockers can also inhibit the afferent and efferent signals in muscle spindles, reducing tremors in essential tremors
  • Commonly used beta-1 blockers include propranolol, metoprolol, esmolol, bisoprolol, and atenolol
  • Adverse effects of beta-1 blockers include bradycardia and decreased cardiac output in patients with decompensated heart failure or super bradycardia.

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