2nd year medical students Alexandria univ.

1. 2ND YEAR MEDICAL STUDENTS
MODULE IX
BY
DR. HAZEM ABO SHOUSHA

2. Main rules
•ABP: pressure of blood on arterial wall

3. ABP= COP X PVR
COP= HR X SV
Main rules

4. HEART RATE
Main rules

5. Main rules
β1 Agonist M2 blocker
β1 blocker M2 agonist
HEART RATE

6. Main rules
BLOOD VESSELS
α1
β2
M3

7. Main rules
BLOOD PRESSURE (Bl.V)
VC
α1 agonist
β2 blocker
VD
α1 blocker
β2 agonist
M3 agonist

8. Main rules
BARORECEPTORS
VD
VC

9. NORADRENALINE
1 1

11. Observation: increased ABP with minimal effect on HR, which increases only with high doses
Explanation of effect of NE on ABP & HR:
 NE acts mainly on 1 receptors  vasoconstriction PVR
 With higher doses of NE, it activates also cardiac 1 receptors some increase in the heart
rate

12. PRAZOSIN
1 blocker

14. What is the effect of Prazosin on ABP and HR?
•it blocks 1 adrenoceptors  vasodilationPVRABP
•ABP slight reflex tachycardia

15. Noradrenaline cause very minimal  in HR  β1 stimulation minimal  in BP

16. 1 β1 β2
ADRENALINE

18. Observation:  ABP & HR
late The ABP  before returning to base line level
Explanation of the effect of epinephrine on HR & ABP
Epinephrine stimulates 1 , 1, 2 adrenoceptors Beta receptors are more sensitive to the effect of epinephrine
On heart: 1 activation  +ve inotropic & chronotropic effects  COP leading to increased
ABP
On BV :
- 1 activation vasoconstriction  PVR.
- 2 activation vasodilatation  PVR

19. •The net effect of these two opposing effects (1 & 2 )
on bl.v is an in  PVR
(1 wins at 1st )
•At High concentration:
EPI stimulates 1
•At Low concentration:
EPI stimulates 2

20. AdrenalineNoradrenalineparameters
More increaseMild or no increaseHeart rate
Less increase than
noradrenaline
More increaseBlood pressure
BP decreases before
reaching base line
Reach base line directlyBP before Base line

21. β1 blocker
Cardioselective beta blocker
ATENOLOL

23. Observation: blocking 1 receptors by atenolol blocks
the effect of epinephrine on HR & decreases the effect
on ABP

24. block alpha1 & beta1 receptors & then inject epinephrine

25. EPINEPHRINE REVERSAL:
The presser effect of epinephrine is reversed due to
1 & 1 blockade, leaving the 2 vasodilating effect acting 
 ABP

26. β1 + β2 blocker
Non-selective beta blocker
PROPRANOLOL

27. How to confirm the cause of epinephrine reversal?
No epinephrine reversal since propranolol blocks not only cardiac 1 receptors but also vascular
2 receptors

28. What is the effect of propranolol on ABP and HR?

29. Propranolol mechanism as antihypertensive:
1-Block β1 in heart so low COP BP
2-  central sympathetic discharge  BP
3- Block β1 in kidney Renin  BP
4- resetting of Baroreceptors  BP
5- Block β2 presynaptic NE release  BP

30. β1 + β2 agonist
Non-selective beta agonist
ISOPRENALINE

32. Observation:
• Isoprenaline increases HR
• Isoprenaline initially decreases ABP.
• As HR reaches its maximum increase, ABP shows minimal increase before returning to normal
Explanation for the effect of isoprenaline on HR & ABP
• Isoprenaline activates mainly beta adrenoceptor
• It activates cardiac 1 receptors leading to increase in HR & force of contraction
(which increases COP)
• Activation of 2 receptors—Vasodilation decrease in PVR
• The net effect of the two factors (COP & PVR) is a decrease in blood pressure
initially.
• However, when force of contraction is markedly elevated, the increase of COP
overcomes the effect of decrease in PVR and thus ABP starts to increase.

33. Design an experiment to prove the explanation for the effect of Isoprenaline on
HR & ABP

34. Observation: atenolol abolishes the effect of
isoprenaline on HR
The initial ABP-lowering effect of isoprenaline is
maintained, while its pressor effect is abolished

35. PROPRANOLOL FOLLOWED BY ISOPRENALINE
Observation: Propranolol blocks 1 & 2 receptors thus abolishes the
effect of isoprenaline on ABP

36. 1 agonist
selective Alpha agonist
PHENYLEPHRINE

37. Observation:
Small dose phenylephrine leads to slight increase in ABP with no effect on HR
High dose phenylephrine increases markedly ABP with decrease in the HR ( reflex bradycardia)

38. Explanation of the effect of phenylephrine on ABP & HR
•Activation of 1 receptors  vasoconstrictionPVR
•High dose of phenylephrine  marked elevation of ABP 
reflex  in sympathetic activity. Parasympathetic activity will
take the upper hand  HR

39. prove the explanation of the effect of phenylephrine on HR
and ABP
Observation: prazosin abolishes the effect of phenylephrine
on ABP & reflex bradycardia disappears

40. prove that reflex bradycardia is due to relative
increase in parasympathetic activity
Observation: decreased HR is abolished by atropine despite of elevation of ABP

41. Nicotinic
Nn , Nm
ACETYLCHOLINE ( Ach )
Muscarinic
M1 , M2 ,M3

43. Observation:
small doses of acetylcholine lower only ABP
Higher doses produce both  in the HR & more
significant lowering of ABP
Explanation for the effect of
acetylcholine on HR and ABP
•on heart: M2 activation  - ve chronotropic effect  COP
•on BV: endothelial cells M3 activation  release of NO from vascular
endothelial cells  vasodilatation  PVR
• Decrease in heart rate & decrease in PVR lead to  ABP

44. Inject ATROPINE & then test the effect of ACETYLCHOLINE

45. ACETYLCHOLINE REVERSAL
1. Inject a test dose of Ach
2. Inject atropine
3.Inject the same dose of acetylcholine
4.Inject a dose of Ach which is 10 times the test dose

46. Explanation for acetylcholine reversal
• Atropine injection  A parasympatholytic blocks muscarinic receptors. It blocks
the effect of small dose of Ach.
• Ach injection [big dose]  Stimulates nicotinic receptors Nn after muscarinic
receptors have been blocked by atropine   ABP
• Due to activation of Nn at :
• Adrenal medulla  release epinephrine  BP
• Autonomic ganglia  release of catecholamines from post-synaptic adrenergic nerve endings
 BP
• The BP by Ach [big dose] after muscarinic receptor block [by atropine]
 Ach reversal

47. oAch reversal by : Nn receptors
oEPI reversal by : β2 receptors

48. Reversible
anticholinesterase
So  Ach ‘ ’augment Ach effect ‘ ’
NEOSTIGMINE

49. prove the mechanism of action of neostigmine