PHYS Vascular Endothelium Flashcards
Effect of ACh on blood vessel endothelium
ACh acts on M receptors -> release of endothelium-derived relaxing factor (EDRF) -> vascular smooth muscle relaxation.
In the case of endothelial cell damage: ACh acts on the M receptors of vascular smooth muscles -> vascular smooth muscle contraction.
NO synthesis within endothelium
ACh/substance P act on receptors -> increase Ca2+ within endothelium -> synthesis of endothelium NO synthase.
NO synthesis converts L-arginine -> L-citrulline. NO is the by-product of this conversion reaction.
Constitutive NO synthase vs Inducible NOS
Ca2+ dependent
Short bursts of release
Present in endothelium & nerves
Ca2+ independent
Longer term release
Present in immune cells
Classify as NO as a EDCF/RF
RF
Classify PGI2 as a EDCF/RF
RF – predominantly for larger vessels with lower resistance
Classify EDHF as a EDCF/RF
(Endothelium Derived Hyperpolarising Factor). RF - predominantly for smaller vessels with higher resistance
Classify angiotensin-II as a EDCF/RF
CF
Classify ECE as an ECDF/RF
CF - Endothelium Converting Enzyme (ECE)
Classify TxA2 as an EDCF/RF
CF - Thromboxane A2 (TxA2)
Classify PGH2 as an EDCF/RF
CF
Classify endothelin as an EDCF/RF
CF - may potentiate function of other contracting factors (EL-1, EL-2, EL-3).
What is the affect of endothelium derived hyperpolarising factors vs hypopolarising factors on blood vessels?
Endothelium derived hyperpolarising factors causes hyperpolarisation of smooth muscle cells
therefore causing dilation. Opposite.
Effect of NO on smooth muscle cell proliferation.
Decreases.