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Life support > CVS Vascular tone and endothelium > Flashcards

CVS Vascular tone and endothelium Flashcards

1
Q

How does vasodilation occur from vasodilator nerves?

A

Vasodilatation occurs as vascular tone
produced by sympathetic vasoconstrictor nerves is inhibited by:
-Parasympathetic vasodilator nerves
-Sympathetic vasodilator nerves
-Sensory(nociceptive C fibres) vasodilator nerves

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2
Q

What do parasympathetic vasodilator nerves release in salivary glands?

A

Release Ach/VIP

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3
Q

What do parasympathetic vasodilator nerves release in pancreas and intestinal mucosa?

A

Release VIP

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4
Q

What does the Ach/VIP released from parasympathetic vasodilator nerves act on and cause?

A

parasympathetic nerves release Ach/VIP act on endothelium to cause
release of NO – vasodilatation in these tissues

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5
Q

What do parasympathetic vasodilator nerves release in male genitalia?

A

Release NO

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6
Q

What does the release of NO by parasympathetic vasodilator nerves do in male genitalia?

A

Release of NO by parasympathetic nerves causes production of cGMP
which leads to vasodilatation

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7
Q

How does sildenafil(viagra) work?

A

Sildenafil (Viagra) enhances this effect of NO by blocking the breakdown of
cGMP by phosophodiesterase 5

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8
Q

Example of sympathetic vasodilator nerves?

A

Skin (sudomotor fibres) – release Ach, VIP

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9
Q

What does it mean by vasodilation being associated with sympathetic-mediated sweating?

A

e.g., Hot weather, exercise
Need more blood flow, to make more sweat,
Need more blood flow to skin
Both help to cool down

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10
Q

How do sensory(nociceptive C fibres) vasodilator fibres work?

A

Stimulation of sensory C-fibre nerves by trauma, infection etc
Release Sub P, CGRP
1) Act on Mast cells to release histamine
2) Act on endothelium and VSM
Both produce vasodilatation called ‘’Flare’’ in skin

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11
Q

What is flare in the skin part of?

A

Flare is part of the Lewis triple response
1) Local redness
2) Wheal
3) Flare

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12
Q

What synthase is NO generated from?

A

Endothelium nitric oxide synthase

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13
Q

What does nitric oxide stimulate to bring about vasodilation?

A

NO stimulates guanylate cyclase(GC) which converts GMP into PKG to bring abouts vasodilation

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14
Q

What is prostacyclin(PGI2)?

A

Endothelium derived relaxing factors

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15
Q

How does PGI2 work to bring abouts vasodilation?

A
  1. Shear stress, inflammatory factors, Ach etc will convert membrane lipids into PGI2 via cyclooxygenase(COX)
  2. PGI2 binds to prostanoid receptor which stimulates the Gs pathway to bring about vasodilation
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16
Q

Why is tonic PGI2 production important in kidneys?

A

Tonic PGI2 production important in maintaining blood flow in renal arterioles

17
Q

What is PGI2 needed in the kidneys to maintain?

A

Needed to maintain glomerular
filtration rate (GFR), and kidney function

18
Q

Why is COX inhibition from NSAIDs dangerous?

A

COX inhibition (NSAIDs), reducing PGI2, is potentially dangerous in kidney failure

19
Q

What are the actions of PKG and PKA in vascular smooth muscle cells?

A

(1) Increase Ca ATPase (SERCA) – increase uptake into SR and exclusion from cell
(2) Increase K channel activity –>
hyperpolarisation –> Decrease VGCCs
(3) Decrease MLCK

20
Q

What is an example of endothelium-derived hyperpolarisation factors?

A

K+

21
Q

How is K+ involved in vasodilation?

A
  1. Shear stress from blod flow, inflammatory factors (Sub P, histamine, bradykinin, Ach) results in the activation of K+ channels
  2. This results in rise in local external K+ levels
  3. This actions on vascular smooth muscle:
    -Switches on K+ channels
    -Increases Na/K-ATPase
  4. This leads to hyperpolarization of VSMCs that causes a decrease in VGCCs and Ca entry
  5. Ultimately leads to vasodilation
22
Q

How do gap junctions work in endothelium-derived hyperpolarisation?

A
  1. Shear stress from blood flow, inflammatory factors (Sub P, histamine, BK), Ach
  2. This results in activation of K+ channels leading to hyperpolarisation
  3. Then there is conduction of hyperpolarization from endothelium to VSMCs which decrease VGCCs and Ca2+ entry
  4. Ultimately leads to vasodilation
23
Q

What does stimulation of beta2-adrenoceptors on vascular smooth muscle result in?

A

Stimulation of beta 2-adrenoceptors
on vascular smooth muscle produces vasodilation in coronary and skeletal muscle arterioles

24
Q

What activity does beta2-adrenoceptor stimulation activate?

A

Beta2-adrenoceptor stimulation –> PKA activity

25
Q

What are the steps that occur once PKa activity is stimulated due to the beta2 adrenoceptor?

A

(1) Increased Ca ATPase (SERCA) – increase uptake into SR/exclusion from cell
(2) Increase K channel activity –> hyperpolarisation –> Decreased VGCCs
(3) Decreased MLCK

26
Q

What can a raised blood pressure cause?

A

Raised blood pressure(hypertension) can cause endothelium dysfunction

27
Q

Why would a raised blood pressure cause a poor cardiac output?

A

It increases afterload:
Poor cardiac output
Heart as to work much harder

28
Q

What is raised blood pressure thought to be due to?

A

Raised blood pressure is thought to be due to an imbalance of
vasoconstrictor and vasodilator mechanisms

29
Q

What type of receptor blocker is Angiotensin II receptor(AT1) antagonist, give an example and how it works?

A

-Gq receptor blocker
-Losartan is an example
-Block AT1 receptors to reduce vasoconstriction

30
Q

What type of receptor blocker is ACEi, give an example and how it works?

A

-Gq receptor blocker
-Enalapril
-Reduce Ang II levels – hypertension, heart failure

31
Q

What type of receptor blocker is alpha 1 adrenoceptor antagonists, give an example and how it works?

A

-Gq receptor blocker
-Prazosin
-Competitive receptor antagonists – drug-resistance hypertension

32
Q

What type of receptor blocker is ETA receptor antagonist, give an example and how it works?

A

-Gq receptor blocker
-Bosentan
-Block ETA receptors which are upregulated in pulmonary artery hypertension

33
Q

What type of blocker is VGCC blockers(CCB), give an example and how it works?

A

-Ca influx blocker
-Amlodipine
-Dihydropyridine subtype, vascular selective, block influx of Ca2+ to reduce
vasoconstriction – hypertension, angina

34
Q

What type of blocker is K channel openers, give an example and how it works?

A

-Ca influx blocker
-Nicroandil
-Hyperpolarisation, less VGCC activation/Ca influx, vasodilatation - angina

35
Q

What are nitrates like glyceryl trinitrate(GTN) and how does it work?

A

-They are contractile mechanism relaxants
NO donors, PKG-mediated vasorelaxations – angina, pulmonary oedema

Life support (38 decks)

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