The Vasculature Flashcards
In which layer of the blood vessels are the endothelial cells?
The tunica intima
In which layer of the blood vessels are the smooth muscle cells?
The tunica media
What are the role of endothelial cells in terms of regulation of smooth muscle constriction/relaxation?
They control the constriction/relaxation of vascular smooth muscle in response to blood bourne factors.
Why do gap junctions exists between epithelial and smooth muscle cells in the different layers of the vasculature?
Which connexin isoform are these gap junctions?
To allow the vessel to respond as a unit irrespective of each cells proximity to the factor mediating contraction/relaxation.
Connexin 43 isoform
Although capillaries contain no smooth muscle so are thought as not able to constrict, which contractile cell type which wraps around the capillary endothelium may potentially regulate capillary diameter?
Pericytes
What is the term given to the passage of blood cells such as leukocytes through venues/capillaries near sites of infection to allow them to enter tissues and mount an immune response?
Diapedesis
What are extrinsic factors that affect vascular tone with examples?
Factors originating outside of the organ/tissue within which that blood vessel is located, such as circulating adrenaline/angiotensin ii and sympathetic nerve stimulation.
What are intrinsic factors that affect vascular tone with examples?
Factors originating from the vessel itself or the organ/tissue surrounding it. These can be:
Endothelial derived from the endothelium - such as nitric oxide (NO) and endothelial-derived hyperpolarisation factor (EDHF) which both cause vasodilation
Myogenically derived from the smooth muscle - such as local hormones, metabolites and other blood bourne substances.
What causes the release of N.O?
ATP C02 Histamine Bradykinin Hydrogen ions
Blood flow! (Therefore there is a basal NO release due to blood flow anyway)
What is the difference between endothelin-1 (ET-1) and endothelium derived hyperpolarising factor (EDHF), both of which are released by the endothelium.
ET-1 causes vasoconstriction
EDHF causes vasodilation
When initiating vasodilation, what do vasodilation factors stimulate when binding to endothelial cells?
An increase in calcium ion concentration.
What does endothelial intracellular calcium bind to in order to for, a complex which stimulated N.O. production?
What molecule produces N.O. and what does it produce it from?
Calcium binds to calmodulin, and as a complex they activate eNOS.
eNOS synthesises N.O. from the amino acid L-argenine.
What happens to the N.O. once it has been produced in the endothelial cells?
It crosses the lipid membrane as it is a gas into the smooth muscle cells. Here it increases concentrations of cGMP which in turn decreases levels of calcium, causing the smooth muscle relaxation and vasodilation expected.
What do the vasoconstriction substances trigger when binding to the endothelial cells of the vasculature?
It stimulates the endothelial cells to synthesise endothelin, which leaves the cell and binds to receptors on the smooth muscle cells which causes cellular contraction via the alpha1 adrenergic receptor pathway (Gq protein = Ip3 and DAG pathway)
How does endothelial derived hyperpolaristion occur?
Vasodilating substances increase endothelial intracellular calcium concentrations, which in turn open calcium activated potassium (K) channels. This causes potassium to leave the endothelial cell and hyperpolarises it, with this hyperpolarisation spreading to the smooth muscle cells via the gap junctions.
