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CVS BM > Blood Vessel Order 6 > Flashcards

Blood Vessel Order 6 Flashcards

1
Q

What are the three layers of blood vessels?

A
  • tunica intima
  • tunica media
  • tunica adventitia
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2
Q

What does the tunica adventitia contain?

A
  • blood vessels
  • fibrous tissue
  • collagen
  • elastin
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3
Q

What is tunica media mainly composed of?

A

predominantly smooth muscle able to contract

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4
Q

What is the tunica intima composed of?

A

Vascular endothelium has the elastic basal lamina as well

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5
Q

What is the vascular endothelium?

A

single cell layer that acts as the blood-barrier interface

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6
Q

What are the functions of the vascular endothelium?

A
  • vascular tone management
  • Thrombostasis
  • Absorption + secretion
  • Barrier
  • growth
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7
Q

What do blood vessels manage pressure dependent on?

A

Shear stress

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8
Q

What are the 5 key molecules?

A

Vasodilator:

  • Nitric Oxide
  • Prostacyclin (PGI2)

Vasoconstrictor:

  • Thromboxane (TXA2)
  • Endothelin (ET-1)
  • Angiotensin 2
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9
Q

What causes the upregulation of nitric oxide?

A

Provision of acetycholine

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10
Q

How is PGH2 formed?

A

1) Phospholipids are converted to Arachadonic Acid by Phospholipase A2
2) This is then converted into PGH2 by the COX enzymes 1 and 2

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11
Q

What is PGH2 a precursor for?

A
  • Prostacyclin via Prostacyclin synthase
  • Thromboxane A2 via thromboxane synthase
  • PGD2/PGE2/PGF2 which = inflammation
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12
Q

What else can Arachidonic Acid fprm?

A

Leukotrienes via lipooxygenase. The lipooxygenase enzyme cascade forms LTA4/LTB4/LTC4/LTD4.
LTD4 causes bronchoconstriction.

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13
Q

What is the mechanism for Nitric Oxide Action?

A

1) NO stimulant binds to G Protein coupled receptor which activates Phospholipase C
2) PLC converts PIP2 —-> IP3 and DAG
3) IP3 moves to the endoplasmic reticulum and stimulates calcium efflux
4) increased intracellular calcium upregulates Nitric Oxide synthetase which forms NO
5) NO exits endothelial cell and moves to smooth muscle
6) In smooth muscle, it upregulates Guanylyl Cyclase activity to form cGMP from GTP.
7) cGMP upregulates protein kinase G which activates potassium channels
8) the potassium hyperpolarises the cell so the smooth muscle cells relaxes

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14
Q

How else can arachidonic acid be formed?

A

from DAG via DAG lipase

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15
Q

What is the mechanism of prostacyclin action?

A

1) PGI2 formed inside the endothelial cell via COX
2) PGI2 leaves cell and binds to IP receptor on smooh muscle cell
3) This is coupled with adenylate cyclase which converts ATP to cAMP
4) cAMP upregulates Protein Kinase A which inhibits Myosin Light CHain Kinase (MLCK) which reduces cross bridge cycling
5) therefore, cell relaxes

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16
Q

What is the other function of prostacyclin?

A

Has anti-platelet properties

17
Q

What is the action of Thromboxane A2?

A

1) Formed in the endothelial cell and diffuses through apical or basement membrane
2) If it binds to alpha receptor = platelets. Beta receptors = vascular smooth muscle
3) Beta receptor is couples with phospholipase C which converts PIP2 to IP3
4) IP3 triggers Ca2+ influx from extracellular space and SER
5) Ca2+ upregulates myosin light chain kinase -> VSMC contracts

18
Q

How is angiotensin 2 formed?

A

1) Renin cleaves angiotensinogen into Angiotensin 1

2) ACE is expressed in endothelial/pulmonary cells and cleaves this to angiotensin 2

19
Q

What is the action of angiotensin 2?

A

1) It diffuses across the endothelium and binds to At-1 receptors on vascular smooth muscle
2) This leads to Phospholipase C activation and therefore conversion of PIP2 to IP3 and DAG.
3) This results in contraction
4) some AT receptors are G protein receptors and are bound to the SRC so upregulate the growth of vascular smooth muscle cells

20
Q

What is the other function of ACE?

A

ACE breaks down bradykinin which is a vasodilator. Bradykinin binds to bradykinin receptors and upregulates the production of NO

21
Q

What is the action of Endothelin 1?

A

1) Endothelin precursor (big-endothelun 1) is produced by the nucleus and cleaved by Endothelin Converting Enzyme to form ENdothelin-1
2) Endothelin-1 then exits endothelial cell and binds to either alpha or beta receptor
3) Both receptors on smooth muscle cause contraction via PLC pathway
4) If it binds to a beta receptor on the endothelial cell, it triggers eNOS production to upregulate NO and stimulate relaxation

22
Q

What are antagonists for the production of the Endothelin-1 precursor?

A
  • Prostacyclin
  • Nitric Oxide
  • ANP
  • heparin
  • HGF
  • EGF
23
Q

What are agaonists for the production of the Endothelin-1 precursor?

A
  • Adrenaline
  • Vasopressin
  • Angiotensi 2
  • Interleukin -1
24
Q

What is the main target of therapeutic pathways?

A

Endothelin-1

25
Q

What are the main therapeutic strategies?

A

1) Inhibit cholinesterase enzyme
2) Inhibit phosphodiesterase enzyme
3) medication including NO groups
4) Block calcium flow into cells

26
Q

What is the mechanism for Nitric Oxide Donors?

A

1) Both endogenous and exogenous No activates guanylyl cyclase that converts GTP to cGMP
2) cGMP activates protein Kinase G that causes relaxation

27
Q

What is the mechanism of viagra?

A

1) cGMP is converted to GMP by phosphodiesterase
2) GMP is metabolically inactive in this pathway
3) Viagra is a phosphodiesterase inhibitor

28
Q

What does Aspiring do to COX enzymes?

A 
COX1 = inactivation 
COX2 = switches function to generating protective lipids
29
Q

What happens at continued low doses of aspirin?

A

Prostacyclin decreases then remains constant whereas thromboxane continuously decreases as platelets are unable to synthesise new COX enzymes

30
Q

What is the effect of ACE inhibitors?

A

Not only the formation of Angiotensin 2 but also we are unable to break down Bradykinin leading to a vasodilatory effect

31
Q

What targets the Gq linked receptor (PLC/PIP2/IP3/DAG)?

A
  • Nitric Oxide production
  • Endothelin-1 action
  • Angiotensin 2 action
  • Thromboxane action
32
Q

What targets the guanylyl cyclase (GTP/cGMP/PKG)?

A

NO action

33
Q

What targets adenylyl cyclase (ATP/cAMP/PKA)?

A

Prostacyclin action

CVS BM (11 decks)

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