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Cardiorespiratory 2 > Nitric oxide in the vascular system > Flashcards

Nitric oxide in the vascular system Flashcards

1
Q

what are the important compounds of nitrogen and oxygen

A
  • Nitric oxide
  • Nitrous oxide
  • Nitrous acid (nitrate
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2
Q

what is the difference between nitrous oxide and nitric oxide

A

Nitrous oxide (N2O) is a mild analgesic “laughing gas”, it is stable and unreactive

Nitric Oxide (NO) is a free radical (a compound with an unpaired electron).

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3
Q

What is Entonox

A

A mix of nitrous oxide 50% and oxygen 50% is a medical anaesthesia gas,

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4
Q

when is Entonox used

A

It is frequently used in pre-hospital care, childbirth and emergency medicine situations

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5
Q

what does NOS stand for

A

nitric oxide synthase

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6
Q

how is nitric oxide synthesised

A

by nitric oxide synthase

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7
Q

what domains does NOS have

A
  • The enzyme has both oxidase and reductase domains
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8
Q

what environmental conditions does NOS require

A
  • has to have oxygen present
  • NO synthesis is inhibited in hypoxic conditions
  • it is enhanced in alkali conditions and inhibited in acidic condition
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9
Q

what does NOS catalyse

A
  • The enzyme converts the amino acid l-arginine into citrulline
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10
Q

what tissues is NOS found in

A
  • Brain
  • Macrophages
  • Vascular endothelium
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11
Q

what are the isoforms of the NOS enzyme

A
  • NOS type I (bNOS or nNOS)
  • NOS type II (iNOS)
  • NOS type III (endothelial NOS, eNOS)
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12
Q

Describe NOS type I (bNOS or nNOS)

A

NOS type I (called bNOS or nNOS)
o Central and peripheral neuronal cells
o Calcium dependent

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13
Q

Describe NOS type II (iNOS)

A

o Most nucleated cells, particularly macrophages
o Independent of intracellular Ca+2
o Inducible in presence of inflammatory cytokines
- part of the immune system

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14
Q

describe NOS type III (endothelial NOS, eNOS)

A

o Vascular endothelial cells

o Calcium dependent

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15
Q

what NOS types require calcium

A

NOS type I (bNOS or nNOS)

endothelial (NOS, eNOS)

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16
Q

What are the main NOS isoforms

A

nNOS and eNOS are the main one and they are similar, and closely related

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17
Q

where else can you find NOS

A

flowing blood

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18
Q

How does shear stress on the endothelial wall cause the entry of calcium ions

A
  • caveolin is dislodged which loosely sits in the calcium channel this allows the entry of calcium ions
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19
Q

describe damage to the endothelium caused by sheer stress

A
  • Shear stress on the endothelial wall caused by the friction of the moving blood flow opens calcium channels (possibly by dislodging a molecule that sits loosely in the calcium channel and blocks. This it called caveolin).
  • The opened calcium channels allow Ca++ into the endothelium
  • Calcium binds to and activates calmodulin, which in turn activates eNOS
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20
Q

what cofactors are involved in the activation of eNOS

A

eg biopterinH4, Flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD) these are enzymes that aid in the oxidation and reduction reactions in NOS

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21
Q

what other factors present in plasma can activate NO synthesis

A

Acetylcholine (& other factors) present in plasma can also activate NO synthesis by binding to acetylcholine receptors on endothelium and opening calcium channels (separate from those activated by shear stress

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22
Q

what does nitric oxide active in the smooth muscle

A

Nitric oxide diffuses from the endothelium into the surrounding smooth muscle and activates guanylate cyclase

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23
Q

what does guanylate cyclase do

A

This converts guanosine triphosphate to cyclic guanosine monophosphate cGMP

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24
Q

what does cGMP do

A

cGMP makes the muscle relax.

- The net effect of raised cGMP is to reduce calcium availability in the muscle and thus inhibit contraction

25
Q

name a function of smooth muscle

A

One of the functions in the smooth muscle is to cause calcium to be sequestered into chambers therefore the muscle relaxes

26
Q

what are the three main groups of cellular targets that cGMP act on

A

cGMP-dependent protein kinases (PKGs), - proteins modified by PKG commonly regulate calcium homeostasis and calcium sensitivity of cellular proteins

cGMP-gated cation channels,

Phosphodiesterates (PDE)s.

27
Q

what is the two main functions of nitric oxide in the vascular smooth muscle

A

1) NO relaxes and dilates arteriolar smooth muscle; this lowers vascular resistance (and prevents hypertension)
2) NO Prevents unwanted intravascular coagulation (eg a DVT/VTE)

28
Q

what does NO do to bronchial smooth muscle

A
  • it relaxes bronchial smooth muscle
29
Q

what does NO work against in the vascular system

A
  • NO synthesis is occurring all the time in a healthy vascular system, and this maintains a low peripheral resistance and a normal blood pressure.
  • It balances the effects of noradrenaline and angiotensin on the blood vessels .
30
Q 
describe how blood flow changes in the
- active muscles
- heart 
- kidney 
- skin 
- brain 
during exercise
A
  1. Blood flow in active muscles increases over TEN FOLD
  2. Heart blood flow increases THREE FOLD
  3. Kidney blood flow DECREASES by nearly half
  4. Skin blood flow increases nearly four fold
  5. brain blood flow does not change
31
Q

what does the sympathetic nervous system tend to do to blood vessels during exercise and what does that mean for vasodilation

A
  • The sympathetic nervous system produces a general vasoconstriction of arterioles in muscle during exercise (mediated by alpha-1 receptors).
  • This tends to reduce local muscle blood flow.
  • However, the muscles which are exercising vasodilate. This implies the presence of a powerful local vasodilator. Active during exercise. - as the vasodilator can overcome the symapathetic global vasoconstrictor tone
32
Q

what are the local vasodilators through to increase blood flow to the exercising muscles

A

adenosine

NO - this is the most important one

33
Q

what it thought to trigger vasodilator during exercise

A
  • acidosis
  • lactic acid is created in exercise when APT is depleted an anaerobic exercise starts
  • this causes many arterioles to open
  • creates acidic conditions for NO to work in
34
Q

what is the problem with NO being released from hypoxic tissue during exercise

A

NOS requires oxygen to make NO therefore how is it possible to make NO in a hypoxic environment
- therefore there must be a storage of NO, but it cannot be in a gas form otherwise it would diffuse out of the tissues

35
Q

how is NO stored

A
  • NO is being constantly synthesized (at low levels) in resting vascular endothelium
  • After the NO has reacted with guanylate cyclase in the muscle it is thought to be converted to nitrous acid and then to nitrite.
  • nitrite can be converted back to NO in hypoxic an acidic conditions
36
Q

show the reaction of NO being converted to nitrite and being converted back to NO

A

NO +. H20 = HNO2 + H+ + e-

HN02 = H+ + NO2-

  • these reactions are reversible
  • have to have a pH of less than 4 for this to work
37
Q

where can nitrite be stored

A

It has been suggested that the endothelium of the arterioles stores nitrite
- (Nitrite anion exists at a concentration of 0.05-1 micromol in blood, and ten times that in vascular endothelium).

38
Q

what causes vasodilator in the coronary arteries

A

This exercise vasodilation is thought to be due to increased nitric oxide in pulmonary venous blood.

  • the endothelium in the pulmonary arterioles is exposed to high PaO2 continually and therefore NOS can work as oxygen is present so NO is produced
  • this NO then travel to the coronary arteries and causes vasodilation
  • this increases during exercise to match the increase workload
39
Q

why is GTN (glycerol trinitrate) good in angina

A

GTN is a good mechanism for angina, as it produces NO and this is good and relaxing coronary vessels

40
Q

what provides evidences that NO is stored as nitrate

A

GTN is a good mechanism for angina, as it produces NO and this is good and relaxing coronary vessels

41
Q

what is GTN used for

A

GTN is an essential drug for treating angina and myocardial infarcts;
- this is because it dilates coronary arteries and opens collateral vessels int he heart which enables blood to get to hypoxic tissue downstream

42
Q

How does GTN work

A
  • GTN is converted to nitrite by mitochondrial enzymes including mitochondrial aldehyde dehydrogenase.
  • Then some other mechanism converts the nitrite to nitric oxide.
43
Q

describe what the effect is of opening collaterals to an ischemic heart

A
  • Some vasodilators like dipyridamole may have a deleterious effect in the ischemic heart as they increase the size of already open blood vessels but do not affect those with atheroma blockage.
  • This shunts blood away from infarcted regions.
  • However nitric oxide from nitrate, by opening collaterals, improves perfusion of ischaemic regions bypassing the blockage
44
Q

what needs to be present for nitrate to be converted back to nitric oxide

A
  • need to be an electron donor (reducing agent) present
  • endothelial cells have been shown to take up the reducing agent ascorbic acid (vitamin C) and this may be the endogenous electron donor
  • vitamin C is good for endothelium supplements and benefits patients with an atheroma and angina
45
Q

describe a use of NO

A
  • some newborns do not have a reduction in pulmonary arterial resistance following the first breath and they suffer from hypoxia as there lungs are not. properly perfused
  • if you add NO to inspired gas it improves the lung function of these children and his drops the pulmonary arterial pressure
46
Q

describe what happens when a baby takes its first breath

A

When the baby takes his or her first breath, the oxygen level in the lungs rises and triggers a massive and rapid synthesis of nitric oxide, which causes relaxation of the vascular smooth muscle and allows vasodilation to occur.
This is the reason for the dramatic drop in pulmonary arterial resistance.

47
Q

what does nitric oxide casein vasodilation in the lung explain

A

This mechanism neatly explains the link between ventilation (pressure of O2) and perfusion.
If ventilation is low, then hypoxic vasoconstriction occurs due to reduced synthesis of NO, due to a hypoxic environment and NOS not being able to work

48
Q

how much does the CO increase during exercise

A

the C.O increases from 5.8 l/min to 17.5 l/min

49
Q

what happens to the pulmonary arterial pressure during exercise

A

The pulmonary arterial pressure increases only slightly.

What happens is that the pulmonary arterial resistance decreases to allow the increased flow in order to match the increase in CO during exercise

50
Q

what causes a decrease in pulmonary arterial resistance during exercise

A

1) The pulmonary arterial walls are thin (they have to withstand only a low pressure), and can stretch easily. Distention in the walls occurs at the start of exercise
2) Increased flow through the pulmonary arterioles may increase nitric oxide synthesis (shear forces increase on endothelial walls), thus making them dilate and lower their resistance.

3) During exercise the sympathetic nervous system acts on beta 2 receptors on bronchial smooth muscle to relax them and increase the bronchial diameter.
- This increased diameter together with a greater tidal volume, increases the oxygen concentration in the alveoli.
- In addition, nitric oxide from the endothelium can diffuse into the alveoli, and thence to the bronchial smooth muscle, increasing bronchial smooth muscle relaxation and airway diameters.

51
Q

what does eNOS do in the pulmonary endothelium

A

The eNOS in the pulmonary endothelium is highly sensitive to the oxygen partial pressure. When the oxygen partial pressure rises, so does the production of nitric oxide.

52
Q

what is the drop in pulmonary resistance mainly due to

A

The drop in pulmonary resistance is mainly due to increased synthesis of nitric oxide in the pulmonary endothelium

53
Q

what does NO do in terms of anticoagulation

A
  • even at rest NO is released from the vascular endothelium in small amounts due to the friction of blood passing over the endothelium
  • This basal release helps prevent leukocytes and platelets from adhering to the surface of the endothelium.
54
Q

why are green vegetables good for us

A

they contain nitrates and ascorbic acid. (especially lettuce, cabbage, broccoli, spinach, watercress etc). Beetroot also contains high amounts of nitrates

55
Q

what happens to nitrates that are eaten

A

These nitrates are converted to nitrites by enzymes in saliva and the nitrites enter the stomach.
In the strongly acid conditions of the stomach the nitrite reacts with the acid to form nitric oxide.

56
Q

what does nitric oxide do in the gastrointestinal system

A
    • is bactericidal and helps kill harmful bacteria in the stomach contents. In addition,
  • the nitric oxide diffuses into the capillary bed of the gastric mucosa and relaxes the vascular smooth muscle, thus increasing stomach blood flow and thus oxygen supply
57
Q

what happens if the stomach acid pH is too high to the nitrites

A

if the stomach pH is too high, the nitrites can pass through the stomach into the small intestine where they can be converted to nitrosamines, which are known to be carcinogenic.
- therefore if you are taking proton pump inhibitors it is advisable to reduce the intake of nitrate containing food

58
Q

name the 5 vascular actions of endothelial NO

A
  1. Direct vasodilation (flow dependent and receptor mediated)
  2. Indirect vasodilation by inhibiting vasoconstrictor influences (e.g., inhibits angiotensin II and sympathetic vasoconstriction)
  3. Anti-thrombotic effect - inhibits platelet adhesion to the vascular endothelium
  4. Anti-inflammatory effect - inhibits leukocyte adhesion to vascular endothelium; scavenges superoxide anion
  5. Anti-proliferative effect - inhibits smooth muscle hyperplasia
59
Q

name 4 things that can happen when NO is impaired

A
  1. Vasoconstriction (e.g., coronary vasospasm, elevated systemic vascular resistance, hypertension)
  2. Thrombosis due to platelet aggregation and adhesion to vascular endothelium
  3. Inflammation due to upregulation of leukocyte and endothelial adhesion molecules
  4. Vascular hypertrophy and stenosis

Cardiorespiratory 2 (43 decks)

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