Physiology of vasculature (3)

Question 1

ET-1 negative feedback mechanism?

Answer 1

ET-1 acts back on EC via ETB receptors to block ECE activity, and to increase NO as shown, to oppose contraction of VSCMs

Question 2

What is AT-II, what is it produced by and where is it predominantly expressed?

Answer 2

Angiotensin II, produced by ACE which is predominantly expressed in EC of pulmonary and renal vasculature
Acts on MAPK pathways in VSMC that cause the SMCs to be more contractile in their responses

Question 3

CV risk factors - why?

Answer 3

Smoking - prevents attachment of eNOS and damages glycocalyx
Ageing - loss of elasticity and compliance of the blood vessels
Hyperglycaemeia - damages glycocalyx and dampens the effect of Akt on eNOS
Hyperlipidaemia - decreases eNOS function, depletes cholesterol storage in calveoli and increases fatty plaque formation
Infection - increased vulnerability to plaque rupture, recruits leukocytes and pathogens, causes inflammation

Question 4

How can ageing impact CV disease wrt blood vessels?

Answer 4

Atherosclerosis
Damage to glycocalyx
Calcification
Loss of elastin
↓ NO (diet, smoking, hypoxia)
Dysreg of contraction due to decreased blood supply to organs
Fatty plaque build up - separates ECs and SMCs causing loss of regulation