Untitled Quiz

Binding of a neurotransmitter to β receptors activates adenylyl cyclase, leading to increased cAMP levels within the cell.

Different tissues primarily express different types of adrenergic receptors. For example, skeletal muscle's blood vessels have both α1 and β2, but mostly β2 receptors; the heart mostly has β1 receptors.

Stimulating α1 receptors causes vasoconstriction, increasing blood pressure and peripheral resistance, especially in skin and abdominal organs.

Stimulation of β1 receptors increases heart rate and contractility.

Stimulation of β2 receptors results in vasodilation, specifically in skeletal muscle blood vessels, and smooth muscle relaxation.

β3 receptors are involved in lipolysis (fat breakdown) and cause relaxation in the bladder's detrusor muscle.

Prolonged exposure to catecholamines reduces receptor responsiveness. This can be due to receptor sequestration, downregulation, or inability to couple to G-proteins.

G protein-coupled receptors that activate cellular responses by initiating a cascade of reactions.

Drugs that stimulate the adrenergic receptors, mimicking the effects of adrenaline.

Reduced responsiveness of receptors to catecholamines (adrenaline-like) after prolonged exposure.

A type of sympathomimetic amine containing a specific 3,4-dihydroxybenzene group.

Rapid breakdown of catecholamines by enzymes (COMT, MAO) in various locations (liver, gut, synapses).

Catecholamines don't readily enter the central nervous system (CNS) because they are polar molecules.

A mechanism of desensitization where receptors are removed from their usual location to reduce activity.

A receptor-desensitization mechanism where the number of receptors decreases (destroyed or not created)

A mechanism of desensitization caused by a kinase attaching phosphate groups to the receptor, impeding interactions with G proteins.

Norepinephrine's effects last for approximately 1 to 2 minutes after infusion stops.

Norepinephrine is broken down primarily by MAO and COMT enzymes, and the inactive products are removed by the body through urine.

Norepinephrine can cause skin discoloration (blanching and sloughing) along the injection vein and tissue damage (necrosis) if it leaks into surrounding tissue. Avoid peripheral vein administration if possible.

Dopamine serves as a neurotransmitter in the central nervous system (e.g. basal ganglia) and is found in the adrenal medulla.

Dopamine activates both adrenergic (α and β) and dopaminergic (D1 and D2) receptors. The differences are crucial for different effects.

At higher doses, dopamine causes vasoconstriction by stimulating α1 receptors.

At lower doses, dopamine stimulates β1 receptors in the heart and also causes vasodilation in the kidneys and other organs (viscera) primarily through D1/D2 receptors.

Dopamine increases blood flow to kidneys by dilating renal arterioles, thereby enhancing glomerular filtration and causing diuresis. It is more beneficial to renal circulation than norepinephrine

Propranolol, as a nonselective β-blocker, reduces heart rate and blood pressure, promoting vasoconstriction in the periphery due to α receptors.

Propranolol lessens the expected heart rate increase during exercise, lowering cardiac output. This occurs because it blocks β1 receptors, damping sympathetic nerve influence.

Propranolol has negative inotropic and chronotropic effects, reducing cardiac output and inhibiting SA and AV nodal activity. This lowers oxygen demand, benefiting angina.

Propranolol can cause bronchoconstriction in susceptible patients due to its blockade of β2 receptors in the lungs. This is dangerous for asthmatics and COPD patients.

Propranolol gradually lowers both systolic and diastolic blood pressure in hypertensive patients, without causing postural hypotension.

Propranolol prevents epinephrine from lowering diastolic blood pressure or increasing heart rate. However, epinephrine's vasoconstrictive action remains intact due to α receptors.

Propranolol is effective in treating supraventricular and exercise-induced ventricular arrhythmias due to its ability to control heart rate and rhythm.

Propranolol blocks β2-mediated vasodilation in skeletal muscles, leading to increased peripheral vascular resistance and reduced blood flow.

Topical β blockers like timolol reduce intraocular pressure (IOP) in glaucoma by decreasing aqueous humor secretion from the ciliary body.

Nonselective β blockers, like nadolol and propranolol, reduce the risk of variceal hemorrhage in patients with portal hypertension caused by cirrhosis.

Beta-blockers that preferentially block β1 receptors, primarily found in the heart, minimizing the unwanted effects on the lungs.

They are used to lower blood pressure in hypertension and increase exercise tolerance in angina (chest pain).

Nadolol, a nonselective β blocker, has a very long duration of action, meaning its effects last for a long time.

Timolol is used topically in the eye to treat chronic, open-angle glaucoma, as it reduces aqueous humor production.

Unlike cholinergic drugs used for glaucoma, β blockers don't affect the eye's focus or pupil size.

Pilocarpine is the preferred drug for emergency lowering of IOP during acute glaucoma attacks.

Propranolol can disrupt glucose metabolism by decreasing glycogenolysis and glucagon secretion. This could lead to a significant drop in blood glucose levels if used alongside insulin.

Propranolol lowers blood pressure by decreasing cardiac output, inhibiting renin release, reducing peripheral resistance with long-term use, and decreasing sympathetic outflow from the CNS.

β-blockers like propranolol reduce intraocular pressure by decreasing the production of aqueous humor in the eye.

Propranolol is effective in managing stable angina by reducing the heart muscle's oxygen demand, thus decreasing chest pain during exertion.

Propranolol and other β-blockers have protective effects against myocardial infarction, reducing infarct size and mortality rate. They potentially achieve this by minimizing the negative impact of circulating catecholamines on the heart.

Timolol, a topical β-blocker, is 5 times more potent than propranolol in reducing intraocular pressure.

While β-blockers can cause hypoglycemia, they can also mask the typical symptoms like increased heart rate and blood pressure. However, sweating (diaphoresis) due to acetylcholine remains.

Propranolol is a versatile drug used for various conditions like hypertension, glaucoma, angina, and myocardial infarction. It works by modulating the sympathetic nervous system and heart function.