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Group of drugs that mimic the actions of norepinephrine and epinephrine which noradrenaline and epinephrine is also known as adrenaline now collectively the and the agents that block the activation of adrenergic receptors are called let’s take a closer look at neurotransmission process in adrenergic first amino acid tyrosine is transported into the neuron by the sodium
Dependent enzyme tyrosine hydroxylase to l-3,4-dihydroxyphenylalanine also known as aromatic amino acid decarboxylase the second step involves transport of converts dopamine to norepinephrine in the third step arrival of the action the neuron the increase in calcium causes the synaptic vesicle to fuse with norepinephrine binds to the postsynaptic receptor on effector organ
Which receptor which results in decrease of norepinephrine release through negative space by diffusing out into the systemic circulation short and most of all norepinephrine gets transported back into the neuron by now once inside the neuron norepinephrine may be either transported recycled or it can be broken down to inactive metabolites by the enzyme that is receptors
Which can be activated by norepinephrine epinephrine and system sympathetic preganglionic neurons release acetylcholine which then binds nicotinic receptors on adrenal medulla now the adrenergic neuron release norepinephrine and about 80 percent epinephrine at the end norepinephrine called alpha and beta now let’s talk about these receptors in more detail and that is alpha-1
And alpha-2 these can be alpha-1c etc but for simplicity let’s just focus on alpha-1 and alpha-2 of thumb when activated it causes stimulatory response mediated by vascular smooth muscle throughout the whole body and when activated they lead when activated they lead to mydriasis which is dilation of pupil they are also urinary retention alpha-1 receptors are also located in
Liver and when glycogen to glucose lastly alpha-1 receptors are also found in the kidney reminder renin is an enzyme that is secreted by the kidney and is involved receptors leads to sympathetic response just think about it when you are in a case you start bleeding you also want to retain urine when you’re fighting or protein-coupled receptors they are primarily located on
Presynaptic nerve camp which in turn leads to inhibition of further release of norepinephrine activated they lead to decrease in insulin secretion now let’s move on to beta-2 and beta-3 unlike alpha receptors beta receptors are coupled with gs mainly located on the heart and when activated they lead to increase heart receptors are also located on the juxtaglomerular cells in
The kidney increase in blood pressure now let’s move on to beta-2 receptors beta-2 and when activated they lead to bronchodilation they are also located on activated they lead to relaxation of blood vessel or in other words and when activated there they lead to smooth muscle relaxation which in gi pancreas and when activated there they lead to increase in insulin secretion
Receptors are mainly located in adipose tissue and when activated they lead to receptors can also be found in the urinary bladder and their activation now let’s switch gears and let’s talk about actual adrenergic agonists so and noncatecholamines as a refresher catecholamine is an organic compound groups intermediate ethyl chain and terminal amine group on the other hand
Groups on adjacent carbons on benzene ring thus the name differences in properties between catecholamines and noncatecholamines talk about how they compare in terms of oral usability catecholamines are enzymes in the gut liver cns and even inside the neurons furthermore hydroxyl poor penetration into the cns now on the other hand we have noncatecholamines substrate for comt
And they’re metabolized by mao very slowly as a action and because they are less polar they also penetrate into the cns fairly easy now there are three types of adrenergic agonists number one direct acting agonists so now let’s take a look at some examples starting with direct acting receptor and mimicking the actions of epinephrine norepinephrine and dopamine and dopamine
Keep in mind that they are non selective meaning they can act on their main route of administration is by injection now one of the most commonly activate almost all adrenergic receptors and because of that it is epinephrine leads to vasoconstriction which in turn decreases mucosal next activation of cardiac beta-1 receptors leads to increase in cardiac patients experiencing
Cardiac arrest caused by asystole lastly activation of epinephrine is sometimes used for emergency treatment of respiratory conditions now what about norepinephrine norepinephrine is actually doses norepinephrine mainly stimulates alpha-1 receptors which leads to norepinephrine has almost no beta-2 activity which is why it has more for norepinephrine are cardiac arrest
And hypotensive shock now let’s talk about beta receptors but also a dopamine receptors and it stimulates them in a receptors only then as dose increases it also activates cardiac beta-1 receptors here as they’re the main target for neuropsychiatric drugs which activating cardiac beta-1 alpha-1 and dopamine receptors found on vascular and hypotensive shock ok so thus far
We talked about non-selective agents which well we actually created selective adrenergic agonists so let’s quickly that are primarily alpha-1 selective best example of these is oxymetazoline of these agents can be found in products used for treatment of nasal congestion redness and phenylephrine due to its ability to raise systolic and diastolic hypotension now let’s talk
About alpha-2 selective drug and here we have a very receptors leads to decrease in sympathetic tone which among other clonidine has also other indications such as attention deficit hyperactivity let’s move on to beta-1 selective agonist best example of this one is cardiac tissue so dobutamine increases cardiac rate and cardiac output which is agonists which stimulate beta-2
Receptors predominant in lungs and lead to have short-acting beta-2 agonists such as for relief of acute asthma symptoms and we also have long-acting beta-2 agonists finally we have beta-3 selective agonist namely mirabegron which to relief of symptoms of over-reactive bladder so that’s it for direct acting group do not directly interact with postsynaptic receptors instead
They enhance the effects of epinephrine or norepinephrine by either these are cocaine and amphetamine which work by blocking reuptake of that controls reward system and this is why they are highly addictive additionally these drugs stimulate alpha-1 and beta-1 receptors which lead to lastly i wanted to briefly discuss mixed action adrenergic pseudoephedrine which cause
Activation of adrenergic receptors by both direct terminals ephedrine and pseudoephedrine have long duration of action because enzymes now primary effects of ephedrine however due to its side effects and availability of better drugs ephedrine bronchial smooth muscle however it mainly activates receptors located in and results in decrease inflammation of nasal passages as
Well as decreased mucus production for this reason sudafed is actually very commonly used enjoyed this video make sure to subscribe and stay tuned
Transcribed from video
Pharmacology – ADRENERGIC RECEPTORS & AGONISTS (MADE EASY) By Speed Pharmacology
