Show Menu

Adrenergic Drugs Cheat Sheet by

Adrenergic drugs summary


Adrenergic drugs
release acetyl­choline at the post synaptic level. Only post ganglionic sypathetic nerves are adrenergic as they use epinep­hrine as neuron transm­itters.
Norepi­nep­hrine is a neurot­ran­smitter of adrenergic synapse, coming from tyrosine → DOPA → Dopamine, stored in vesicles until it needs to be released, when impulses from CNS send the signals. They use exocytosis so the norepi­nep­hrine gets into the synaptic cleft. In synaptic cleft, norepi­nep­hrine needs to act on post synaptic receptors.
Norepi­nep­hrine is released from the presyn­aptic membrane 1) Most of it is taken back w/out any changes to be reused (uptake 1),
2) Taken by factors cells AKA non neuronal uptake (uptake 2)
3) Diffuse
4) Degrade (by enzyme present in the synaptic left, minor).
Norepi­nep­hrine can act on presyn­aptic receptors, regulate release of Norepi­nep­hrine from sympat­hetic nerve endings (AKA alpha 2 recept­ors), regulates -ive feedback mechanism (uptake 1)

Drugs - based on potency

Norepi­nep­hrine → epinep­hrine → isopre­naline
Isopre­naline → epinep­hrine → norepi­nep­hrine
α,β adreno­ceptors
Epinep­hrine + norepi­nep­hrine

Groups of drugs

Mechanism of action
α1 adreno­ceptors
Postsy­naptic - mediate effect on sympat­hetic nerve system (smooth muscle tissues + organs + blood vessels))
α2 adreno­ceptors
Presyn­aptic - out of synapse (mediat effects on catech­ola­mines released from adrenal medulla)
β1 adreno­ceptors
Postsy­naptic - mediate effect on sympat­hetic nerve system (heart)
β2 adreno­ceptors
Presyn­aptic - out of synapse (mediate effects of catech­ola­mines ccircu­lating in blood leads to vasodi­lation)

Adreno­-po­sitive drugs

α, β-adre­nom­imetics (natural - used intrav­eno­usly)
Epinep­hrine, norepi­nep­hrine
α-adre­nom­imetics (selec­tive)
α1-adr­eno­mim­etics = phenyl­ephrine (increases BP locally + effective orally)
α2-adr­eno­mim­etics = Naphaz­oline, clonidine (decreases BP, antihy­per­tensive drug)
β-adre­nom­imetics (selec­tive)
β1,β2-­adr­eno­mim­etics = isopre­naline
β1-adr­eno­mim­etics = dobutamine (if patient doesnt have hypoxia or ischemic disease)
β2-adr­eno­mim­etics = salbutamol (short acting drug), phenoterol, salmeterol (slow/­pro­longed acting drug)
Sympat­hom­imetics (indirect binding on receptors)
Ephedrine (acts on sypathetic endings, stimulates release of norepi­nep­hrine, indirectly produces efftecs on post synaptic receptors)

Adreno­-ne­gative drugs

Adreno­blo­cke­rs/­adr­eno­ceptors antago­nists (direct binding on receptors)
α, β-adre­nob­lockers (natural) - Labetalol
α-adre­nob­lockers - α1,α2-­adr­eno­blo­ckers (non-s­ele­ctive) - Phento­lamine, dihydr­oer­got­amine
α1-adr­eno­blo­ckers -
α1a-ad­ren­obl­ockers - tamsulosin
α1b-ad­ren­obl­ockers - prazosin
β- Adreno­blo­ckers / adreno­ceptor antago­nists
β1,β2-­Adr­eno­blo­ckers (non-s­ele­ctive) - Propra­nolol, timolol
β1-adr­eno­blo­ckers - atenolol, metrolol
Sympat­hol­ytics (indrect binding on receptors)
Reserpine, guanet­hidine

Indica­tions + side effects

α adreno­mim­etics
Pharma­col­ogical effects - Vasoco­nst­riction of blood vessels
Decrease NA peripheral
β adreno­mim­etics
Indica­tions - Bronchial asthma, uterine relaxation (prese­rving pregnancy)
pharma­col­ogical effects - cause dilation of brochial passages,
Vasodi­lation in muscle and liver,
Relaxaion of uterine muscle,
Release of insulin
α adreno­blo­ckers
Side effects - hypote­nsion
β adreno­blo­ckers
Mechanism of action of antihy­per­tensive action of beta adreno­blo­ckers - decrease cardiac output
Decrease renin secretion
reduce central sympat­hetic activity (selective BB))
Side effects
Side effects β2 AB
- Heart insuff­iciency, bronch­oco­nst­riction, *hypog­lyc­emia*, fatigue, dizziness, nausea, diarrhea
Side effects β1 AB -

Specific drugs

Phento­lamine (anatg­onises α1+2 adreno­cep­tors)
Decreases BP caused by adrena­line, affects -ive feedback mechanism (α2-ad­ren­oce­ptors) in the synapse
Indica­tions - Pheoch­rom­ocytoma (adrenal gland tumour) + endart­eritis (infla­mmation of arteries, legs
Side effects - Orthos­tatic (standing) collapse (severe drop in BP) + tachyc­ardia
reverse effects of adrenaline on BP
Tamsulosin (Selec­tively anatgo­nis­es/­blocks α1A-ad­ren­oce­ptors)
Indication - benign prostate hyperp­lasia (increased cell production in a normal tissue or organ)
Relax smooth muscle of prostate gland
Help to decrease these symptoms
Prazosin (Selec­tively atango­nis­es/­blocks α1B-ad­ren­oce­ptors in bood vessels)
Does not affect the -ive feedback mechanism in synapse
Indication - arterial hypert­ension
Side effect - othostatic collapse

Specific drugs

Propanolol - Non-se­lective β1,β2-­adr­eno­blocker
Decrease heart output, decrease activity of SA + AV nodes, decrease BP due to action on:
Heart - decreases heart output
Kidney (propa­nolol decreases production production of renin in the kidney
CNS (decrease sympat­hetic activity on PNS))
Atenolol, Metoprolol (Selective β1-Adr­eno­blo­cker)
Cardio­sel­ective in therap­eutic doses
drugs of choice in cardiac patients


No comments yet. Add yours below!

Add a Comment

Your Comment

Please enter your name.

    Please enter your email address

      Please enter your Comment.

          More Cheat Sheets by FCGLITCHES

          Cholinomimetics Cheat Sheet