1. Pharmacological actions of cathecholamines
Dr Adedunni Olusanya

2. Objectives Identify cathecholamines
Understand their mechanism of actions

3. Cathecholamine -Intro
Made up of a benzene ring
Linked to 2 hydroxyl group and an amine group
Includes dopamine, norepinephrine and epinephrine
Same synthetic pathway – tyrosine is the precursor

4. Cathecholamines
Dopamine – a precursor of other cathecholamine, synthesised in the cytoplasm and stored in vesicles or converted to NE
NE – synthesised and stored in vesicles and adsorbed on chromagrannin as a complex with ATP
Adrenalin – formed from NE by glucocorticoid induction of N- methyltransferase in the adrenal medulla. NE diffuses into the cytoplasm where it is converted to Adr by the methylating enzyme

5. Pharmacokinetics Orally inactive
Rapidly metabolized by MAO and COMT in the intestinal wall and the liver – very low bioavailability
Hence given parenterally

6. Dopamine Precursor of other naturally occurring catecholamine
Major neurotransmitter in the basal ganglia, limbic system, chemoreceptor trigger zone and other parts of the CNS
Peripherally acts on renal and mesenteric endothelium

7. Dopamine (contd) Agonist at D1, D2, A1 and B1 receptors
Main effect is on vascular tissue
A1 adrenergic receptors - vasoconstriction at high doses
B1 and D1 receptor - positive inotropic effect
D 1 receptor- dilation of renal and mesenteric vessels

8. Blood pressure - increases systolic BP
No effect on diastolic BP

9. Clinical uses
Severe heart failure
To increase BP and urine outflow

10. Adrenaline
Heart - Increases heart rate, conduction and contraction via beta 1
Blood vessel –
Vasoconstriction in cutaneous, mucous membrane and renal bed via alpha 1
Dilation in skeletal muscles, livers and coronary vessels via beta 2
No direct effect on cerebral blood vessel
Blood pressure
Increase in systolic BP
Decrease in diastolic blood pressure
Decrease in peripheral resistance
A moderate increase in mean BP

11. Adrenalin Respiration Git and bladder
Bronchodilation via beta 2
Decongestant on bronchial muscle via alpha one
Git and bladder
Relaxation of smooth muscles – alpha 1, beta 2 , constriction of sphincters- Alpha 1
Uterus – Relaxation B2
Contraction – Alpha 1

12. Adrenalin contd Skeletal muscle – Metabolic effects –
Adrenalin augments Ach release via alpha 1 receptors (heteroceptors).
On muscle fibres – B2 shortens the active phase of contraction and reduced tension is developed in the slow contracting red fibres as well as increased firing of muscle spindles – tremors.
Metabolic effects –
glycogenolysis leading to hyperglycaemia in the liver - B2 ,
muscle glycogenolysis leading to hyperlacticidaemia – B2
Fats lipolysis – B1, B2 , B3
Mild effect on insulin secretion – B2
Renin increase via B1

13. Adverse effects and contraindications
Transient restlessness, tremors, anxiety, tremors and pallor
Transient hypertension
Contraindicated in hypertensive, hyperthyroid and angina patients
Contraindicated with halothane use – arrhythmia
Contraindicated in patients on Beta blockers- dangerous hypertensive crises may develop because of unopposed alpha blockade

14. Clinical uses
Cardiac stimulant
Local vasoconstrictor

15. Noradrenaline
Similar to adrenalin but because of its very low to absent effect on B2 , some differences
Blood pressure – Increases both systolic and diastolic ,
Increased peripheral resistance and mean arterial BP
Reduce heart rate – Causes higher blood pressure hence more likely to cause vagal stimulation.
Blood vessels – reduced blood flow due to A1 effect on skeletal, skin and mucous membrane and renal vessels
No effect on bronchial smooth muscle,
GIT, Bladder – relaxation of muscle, contraction of trigone
Metabolic effects – insulin secretion inhibited by A 2

16. Clinical uses of noradrenaline
Rarely used