Endothelial Function Flashcards
Why is smooth muscle growing in blood vessels a bad sign?
Can lead to blockage
Smooth muscle can change from contractile > synthetic
What are relaxing agents?
NO
PG’s (Prostacyclin)
What are the contracting agents?
Endothelin I Angiotensin II (ACE turns angiotensin 1 > 2 = strong vasoconstriction)
How is Prostacyclin derived and what does it do?
- derived from AA by PGHS
- inhibits platelet aggregation via cAMP
- relaxes smooth muscle via cAMP
- inhibits prolif. of vasc. smooth muscle
How is NO derived and what does it do?
- produced by endothelium
- inhibits platelet aggregation via cGMP
- relaxes smooth muscle via cGMP
- inhibits prolif. of vasc. smooth muscle
- locally acting
- implicated in pathological states (superoxides from oxidative stress can inactivate it)
What does Endothelin I do?
- no effect on platelets
- most potent vasoconstrictor
- stimulates prolif. vasc. smooth muscle
- implicated in pathological states (hypertension)
What does nitric oxide synthase (NOS) do?
Synthesises NO from L-arginine
What are the 3 types of NOS?
1) ec NOS
- Endothelial isoform
- Ca dependent
- Produces NO in response to ACh + shear stress
2) n NOS
- Neuronal isoform
- Ca dependent
3) i NOS
- Ca independent
- Expression induced by exposure to inflam.
What effect does oestrogen have on vascular smooth muscle relaxation?
Premenopausal oestrogen = cardioprotective > stimulates endothelial cells to release NO
Post menopause = increased risk HD
What are the uses of NO?
- kills bacteria in macropages
- communication between neurons (NANC = thought uses as NT)
- egg fertilisation
- pulmonary hypertension (dilates BV in lungs)
How does NO work?
Binds to soluble guanylate cyclase = increased cGMP/PKG = reduces IC Ca = smooth muscle relaxation
Describe atherosclerotic classification
- eccentric
- lumen deforming
- fibrous intimal cap
- fibrous elastinolysis
- vessel stiffening
Describe medial calcification
- concentric
- medial fibrosis + elastinolysis
- adventitial inflammation
- vessel stiffening