8: SNS agonists Flashcards
Where are a1 adrenoreceptors located?
What is their second messenger mechanism and prinicpal effect?
Alpha 1 receptors:
- Eye (contraction of iris dilator muscle)
- vasoconstriction (SM constriction)
- excretion of nose
- contraction of ureter–> holding urine
–> Exitory via
PLC into IP3 and DAG
Where are alpha 2 adrenorecpetors commonly found?
What is their secound messenger system and principal effect?
Usually inhibitory –> decerease of cAMP
- regulation in CNS
- reduction of aqueous humor production in ciliary body
Where are ß1 receptors located?
What is their secound messenger system?
Heart –> icrease heart rate + force of contraction
Kideny–> increase renin –> increase reabsorbtion
Messenger System: increase in cAMP
Where are ß2 adrenoreceptors located?
What is their 2nd messenger system
Bronchios/Airway
Vessels –> causing vasodilation
uterine smooth muscle
increase in cAMP
How would you medically treat an anaphylactic shock?
What are the (desired) effects?
Adrenaline (non-selective adrenoreceptor agonist) e.g. in Epipen
It counteracts the problems associated with too much histamine release:
- ß2–> Bronchiodilation
- ß1 –> tachycardia
- a1 –> vasoconstriction
- Might bind to ß receptors on mast cells and supresses the release of mediator cells
–> to increase BP and maintain breathing
What do you use adrenaline for? (as drug)
- Anaphylactic shock
- Emergency Astmah + acute bronchspasm (ß2)
- Cardiogenic shock (ß1)
- Maintaining BP during spinal anestehsia (a1)
- Prolonging effect during local anesthesia (a1)
What are the side effects of Adrenaline use?
When might this be problematic?
- Reduces and thickened secretions
- Tremor (skeletal muslce)
- CVS effects
- tachycardia, palpitation, arrythmias
- vasoconstriction (cold extremities)+ high BP
- at overdose: cerebral haemorrhage and pulmonary oedema
- (Minimal CNS and GI effects)
Overall: not too severe, only in elderly patients of with underyling condition (e.g. heart problems)
What are COMT and MAO?
Where are they situated
Both enzymes that break down Adrenaline/Noradrenaline
Catechol-O-Methyltransferase –> More peripheral
MAO –>Monoaminooxidase = More in CNS
Which drug is a a1 selective agonist?
More or less selective:
Phenylephrine
What is the mechanism of action and the clinical use of Phenylephrine?
It is a (more or less) a1 selective adreno agonist
It is more resistant than Adrenlaine to COMT –> longer there than Adrealine itself
- vasoconstriction
- Mydriasis
- Nasal decongestant (abschwellendes Mittel)
- vasoconstriction –> less fluid production
Which drug is used as a a2 adrenergic agonist?
Clonidine
–> a2 receptors are inhibitory!
- Glaucoma (decrease of humous production due to stimmulation of a2 receptor)
- Treatment in hypertension and migrane
- Reduction of sympathetic tone (by reducing sympathetic outflow via binding to a2 receptors in brainstem that then reduce signaling –< presynaptic inhibition of Noradrenline release)
What are the clinical uses for Clonidine?
More or less selective a2 adrenoreceptor agonist
a2 receptors are inhibitory!
- Treatment of Glaucoma (decrease of humous production due to stimmulation of a2 receptor)
- Treatment in hypertension and migrane
- Reduction of sympathetic tone (by reducing sympathetic outflow via binding to a2 receptors in brainstem that then reduce signaling –< presynaptic inhibition of Noradrenline release)
Which adrenorecepors controll vascular tone in the brain?
ß2 receptors–> would not want vasoconstriction to the brain
What is an example of a adrenergic ß receptor selective drug?
Isoprenaline
- more resistant to break down by MAO (central effects) and uptake 1 than Adrenaline
When would you use Isoprenaline as medication?
What is the problem with the use of isoprnaline?
It is a adrenergic ß receptor selective agonsit (ß1=ß2)
Used in:
- Cardiogenic shock
- Acute heart failure
- MI
Can be problematic: (especially in e.g. Astmah medication when patients would always get refelx tachycardia)
- stimmulation of ß2 receptors causes vasodilation
- –> drop in BP
- Causing reflex tachycardia (via Baroreceptors)
What is the clinicl use of Salbutamol?
Explain the mechanism of action and unwanted effects
Salbutamol –> increase in cAMP –> increase in PKA
- Main use in astmah
- side effects
- Cardiac–> increase in BP, tachycardia, arrythmias
- hyperglycaemia
- tremor, restlessness
