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Observation: increased ABP with minimal effect on HR, which increases only with high doses 3
Explanation of effect of NE on ABP & HR: NE acts mainly on E1 receptors VSM contraction vasoconstriction (skin, mucous memb., splanchnic area) PVR With higher doses of NE, it activates also cardiac F1 receptors some increase in the heart rate
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Observation: ABP & HR The ABP before returning to base line level
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net effect of these two opposing effects (E1 & F2 ) on vSMC is an in PVR. y At lower epinephrine concentrations, the effect on alpha receptors decreases, while the activity on F2 receptors predominates leading to decrease PVR & lowering ABP before returning to base line level
y The
Design an experiment to demonstrate the role of F1 receptors in the effect of adrenaline on HR & ABP
Observation: blocking F1 receptors by atenolol blocks the effect of epinephrine on HR & decreases the effect on ABP
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What happens if you block alpha & beta receptors & then inject epinephrine?
No epinephrine reversal since propranolol blocks not only cardiac F1 receptors but also vascular F2 receptors12
Observation: In equimolar doses of epinephrine & NE: Only epinephrine increases HR NE produces higher increase in ABP
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Explanation
y
NE acts mainly on alpha receptors with minimal effect on beta receptors minimal increase in HR Absence of F2 dilating effect explains why the PVR and ABP is more by norepinephrine.
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3rd experiment: effect of different doses of isoprenaline (Beta agonist) on HR & ABP
Observation: Isoprenaline increases HR Isoprenaline initially decreases ABP. As HR reaches its maximum increase, ABP shows minimal increase before returning to normal
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Isoprenaline activates mainly beta adrenoceptor It activates cardiac F1 receptors leading to increase in HR & force of contraction (which increases COP) Activation of F2 receptorsVasodilaton 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.
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Design an experiment to prove the explanation for the effect of isoprenaline on HR & ABP
y
Observation: atenolol abolishes the effect isoprenaline on HR The initial ABP-lowering effect of isoprenaline maintained, while its pressor effect is abolished
of is
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Design an experiment to prove the explanation for the effect of isoprenaline on HR & ABP Step 2: inject propranolol to block F2 receptors followed again by isoprenaline
Observation: Propranolol blocks F1 & F2 receptors thus abolishes the effect of isoprenaline on ABP
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Observation: Small dose phenylephrine leads to slight increase in ABP with no effect on HR High dose phenylephrine increases markedly ABP with 19 decrease in the HR
Design an experiment to prove the explanation of the effect of phenylephrine on HR and ABP
y
Observation: prazosin decreases or abolishes the effect of phenylephrine on ABP & reflex bradycardia disappears21
How to prove that reflex bradycardia is due to relative increase in parasympathetic activity
heart: M2 activation
COP
- ve
chronotropic effect
y on BV: endothelial cells M3 activation release of NO from vascular endothelial cells vSMC relaxation PVR y Decrease in heart rate & decrease in PVR lead to ABP
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Observation: small doses of acetylcholine lower only ABP Higher doses produce both in the HR & more significant 24 lowering of ABP
Design an experiment to prove the explanation of the effect of acetylcholine on HR & ABP
y
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Inject a test dose of acetylcholine Inject atropine Inject the same dose of acetylcholine Inject a dose of acetylcholine which is 10 times the test dose
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Observation: Neostigmine increases the ABP- lowering effect of acetylcholine & augments its effect on HR
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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 Rise in ABP Due to activation of NN at :
Adrenal medulla release epinephrine BP Autonomic ganglia release of catecholamines from postsynaptic adrenergic nerve endings [sympathetic predominance] BP
The BP by Ach [big dose] after muscarinic receptor block [by atropine] Ach reversal
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