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PN3312 > Vasodilation > Flashcards

Vasodilation Flashcards

1
Q

What is vasodilation?

A

Relaxation of the vascular smooth muscle (vascular - associated with blood)

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2
Q

What is the structure of a blood vessel?

A
  • Tube (lumen) surrounded by smooth layer of muscle

- Inside of blood vessel has a layer of endothelium

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3
Q

What is angina?

A
  • Plaque in blood vessels of the heart, and so unable to get enough oxygen to the muscles of the heart and so cannot relax properly
  • Results in chest pain
  • Important cause of cardiovascular death
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4
Q

How did Robert Furchgott investigate vasodilation?

A
  • Tension device connected to ring of aorta from rabbit in organ bath
  • Contract first with noradrenaline and then adding acetylcholine to see relaxation
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5
Q

What results did Furchgott obtain?

A
  • Non reproducible results

- Either a steep decrease in tension with acetylcholine or high tension until very high conc of acetylcholine

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6
Q

What was the cause of Furgott’s results?

A
  • Student accidentally removing endothelium from aorta
  • Therefore Ach was not acting directly on muscles but on endothelium, idea introduced of endothelium derived relaxing factor (EDRF)
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7
Q

What evidence was supplied by Ignarro and Salvador Moncada that NO was EDRF?

A
  • Small molecule that can diffuse quickly

- Can activate guanylate cyclase as free radical binds stongly to Fe in haem group of molecule

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8
Q

What is the proposed mechanism of vasodilation?

A
  • Arrival of Ach causes Ca2+ channel to open
  • Ca2+ activates NO synthase which acts upon Arganine and Oxygen to produce citrulline and nitric oxide
  • Nitric oxide binds to guanylate clyclase activating it
  • Conversion of GTP to cGMP which acts as a protein kinase inducing relaxation
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9
Q

Why is the synthesis of NO through arganine unlinkely?

A

Uses oxygen, vasodilation used to deliver more oxygen to tissue

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10
Q

What is an alternative explanation for the source of NO? What evidence exists of this?

A

(NO2-) (nitrite) -> NO

  • Always present in blood plasma, conversion not difficult to effect
  • Fall in nitrite content between arteries and veins (however very little)
  • Higher concs of nitrite in Tibetan highlanders (stronger evidence but still not entirely proven)
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11
Q

What alternative explanation exists for the synthesis of NO aside from NO2-?

A

S-nitothiols (formula RSNO) decompose 2 RSNO -> RSSR +2NO

S-nitrocysteine and S-nitrogulathione circulate in the blood

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12
Q

What did Jonathan Stamler propose the mechanism for NO?

A

Nitric oxide carried by haemoglobin in the cysteine residue (conserved in many species with no obvious use) to give SNOHb
However:
Probably not correct as rat with induced human haemoglobin without cysteine residue shows no fatigue effects

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13
Q

How is NO involved with blood clotting?

A

Prevents platelet aggregation and cohesion (procued by eNOS)

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14
Q

What is the involvement of NO in the immune system?

A
  • Found that participants who have had fevers have high ammounts of nitrate in their urine
  • NO reacts with superoxide in lysosome to for peroxynitrate which is then converted to nitrate and excreted
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15
Q

What is the role of NO in respiration?

A
  • Nitric oxide binds to Fe4S4 clusters ending respiration and leading to necrosis
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16
Q

What is the role of NO in the brain?

A
  • Glutamate is the neurotransmitter
  • Binds to NMDA receptor
  • Opens channels to allow calcium ions to flow into the postsynaptic neurone
  • Stimulates nNOS to convert arginine into NO
  • NO diffuses back, reaching not only presynaptic neurone but many others, mechanism in memory could decay with age?
17
Q

What is the role of nitric oxide in the peripheral nervous system?

A
  • NANC nerves (non-adrenergic non-cholinergic) have NO as their transmitter
18
Q

What are the properties of H2S?

A
  • Extremely toxic
  • Bad odour
  • At physiological pH present a the hydrogen sulphide ion (Hs- + H+)
  • Obtained from cysteine by 3 enzyme: CBS, CSE and 3-MST and is also manufactured by intestinal flora
  • Reacts with another HS group to form S-S bond (sulfhydration)
19
Q

What are the roles of H2S in the cardiovascular system?

A
  • CSE knockout mice show hypertension and impaired vasodilation
  • Enhances Katp channels
  • Disregulated H2S biosynthesis associated with maternal hypertension and pre-eclampsia
20
Q

What is the role of H2S in the gut?

A

CBS, CSE and 3-MST manufactured by resident microbes

Role in smooth muscle relaxation, protection against inflammation, damage and alcohol induced gastritis

21
Q

Where is H2S found in the nervous system?

A
  • CBS found in the glia
  • CSE and 3-MST found in neurons
    Multiple sources indicate importance
22
Q

What is the proposed role of H2S in the nervous system?

A
  • Long term potentiation likely involves sulfhydration

- Disregulation of H2S metabolism occurs in Alzheimers and Parkinsons

23
Q

How are H2S and NO synergistic?

A
  • In aorta low concentrations of H2S greatly augments NO induced smooth muscle relaxation
  • Reducing CSE activity reduces response of NO donors and vica versa
  • Vasodilatory effect of H2S is lost in eNOS knockout mice
24
Q

Give an example of H2S and NO direct chemical reaction

A
  • Enzymes producing these compounds are co-located
  • H2S can react with nitrosothiol to give HSNO (thionitrous acid the simplest and first nitrosothiol, possible vasodilator) however this degrades at 12K so probably not
  • HSNO does ionise however to give H+ and -SNO
25
Q

What does the reaction between NaSH and NO give?

A

HSSNO (perthionitrite) - More stable than HSNO
NO,
NO- (nitroxyl),
OH-N(O)-SO3
polysulfide - sulfiure likes to catenate (link with itself to form rings) used by the body and biologically active vasodilators with significantly different effects
- Possible therapeutic benefit of NaHS? Not been shown in vivo

26
Q

What is synergy?

A

Otherwise known as ‘cross-talk’
- Modulation of enzymes belonging to the same signalling pathway by reciprocal functional interaction or direct chemical reaction

PN3312 (11 decks)

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