endothelial cell function 5.2 Flashcards

(20 cards)

1
Q

what are the types of major arteries

A

Elastic (central) - aorta, iliac

muscular (conduit) - femoral, radial, popliteal. cerebral, coronaries

resistance - arterioles

exchange - capillaries

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2
Q

what are the parts of the artery

A

tunica externa - collagen fibres and elastic tissues

tunica media - vascular smooth muscle cells, collagen fibres and elastic fibres

tunica intima - basement membrane, endothelial cells

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3
Q

what trends do you notice with vasculature make up

A

as you get closer to the tissues, there will be less elastic tissue, smooth muscle, and fibrous tissue, but endothelium remains the same

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4
Q

Why are resistance arteries (arterioles) essential in regulating blood pressure and blood flow distribution?

A

Resistance arteries account for >80% of total resistance to blood flow in the arterial system.
They reduce the high pressure coming from larger conduit arteries before blood reaches capillaries.
By adjusting their diameter, they regulate systemic blood pressure and control where blood is distributed throughout the body.
Their branching structure progressively decreases vessel size, ensuring proper delivery to tissues.

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5
Q

What regulates arterial diameter, and why is vascular tone important?

A

Endothelial cells play a central role in regulating arterial diameter.
Blood vessels maintain vascular tone, meaning they are never fully dilated and always slightly contracted. This helps:

Regulate blood pressure
Direct blood flow to different tissues based on physiological needs.
Regulation involves signals such as:

Shear stress
Neural signals (ACh)
Humoral factors (e.g., insulin)

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6
Q

How does endurance training affect blood flow and oxygen delivery to skeletal muscle?

A

Endurance training increases blood supply to skeletal muscle.
This occurs through adaptations such as:

Increased red blood cell count, improving oxygen‑carrying capacity (though also increasing viscosity)
Higher capillary density, enhancing oxygen delivery and waste removal..

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7
Q

what causes vasoconstriction

A

Increased sympathetic activity
Norepinephrine, ATP, NPY
ATP
NPY

Hormone responses
Epinephrine/norepinephrine
Angiotensin II
Endothelin-1

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8
Q

what causes vasodilation

A

Increased vagal activity
Acetylcholine,
Increased shear stress
Metabolite accumulation
(lactate, H+, ATP)
Hormone responses
Estrogen/testosterone, insulin,VEGF, etc.

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9
Q

how can app lead to both vasoconstriction and vasodilation

A

it can work on different receptors, and where they are located. Receptors located on muscle cells, causes vasoconstriction (P2X receptor). Receptor on endothelial cell causes vasodilation (P2Y receptor)

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10
Q

How does Endothelin‑1 (ET‑1) released by endothelial cells regulate vasoconstriction and vasodilation?

A

ET‑1 is continuously produced by endothelial cells, but its production can be increased when needed.
ET‑1 is released into the space between endothelial cells and vascular smooth muscle cells (VSMCs).
Binding to ETA and ETB receptors on VSMCs → increases Ca²⁺ → causes contraction → vasoconstriction.
Binding to ETB receptors on endothelial cells → stimulates nitric oxide (NO) release → counteracts constriction → vasodilation.

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11
Q

How do endothelial cells produce nitric oxide (NO), and what activates eNOS?

A

Nitric oxide synthase (eNOS) in endothelial cells produces NO.
Calcium (Ca²⁺) is required for most signaling inside the endothelial cell and is crucial for activating eNOS.
When stimulatory signals (e.g., shear stress, agonists like ACh) increase intracellular Ca²⁺, Ca²⁺ binds calmodulin, which activates eNOS.
Activated eNOS converts L‑arginine → nitric oxide (NO).
NO then diffuses to smooth muscle cells and causes vasodilation.

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12
Q

What is nitric oxide (NO), and why is it important in vascular physiology?

A

Nitric oxide is a very potent vasodilator.
It is a gas with a very short half‑life (seconds).
NO is a reactive nitrogen species, meaning it has an unpaired electron and reacts quickly with surrounding molecules.
Its main vascular function is to relax smooth muscle and increase blood vessel diameter.

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13
Q

Which enzymes produce nitric oxide, and which form is most important for blood vessels?

A

NO is produced by three nitric oxide synthase (NOS) enzymes:

nNOS (NOS1) – neuronal
iNOS (NOS2) – inducible
eNOS (NOS3) – endothelial.

The enzyme most relevant for vascular control is eNOS, found in endothelial cells.

nNOS and eNOS produce small amounts of NO using calcium, while iNOS produces large amounts when activated.

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14
Q

How does BH4 influence eNOS activity and nitric oxide (NO) production?

A

eNOS requires BH4 (tetrahydrobiopterin) to be “coupled.”
When eNOS is coupled, it correctly converts L‑arginine → nitric oxide (NO).

If BH4 levels are low, eNOS becomes uncoupled, meaning it produces superoxide (a harmful reactive oxygen species) instead of NO.

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15
Q

How does nitric oxide (NO) cause blood vessels to relax?

A

NO is produced by endothelial cells and diffuses into nearby vascular smooth muscle cells.
Inside the smooth muscle, NO activates guanylyl cyclase, increasing cGMP levels.
cGMP reduces intracellular calcium and activates pathways that relax the smooth muscle, causing vasodilation.
Result: the blood vessel widens, lowering resistance and improving blood flow.

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16
Q

What is shear stress in blood vessels, and why is it important?

A

Shear stress is the frictional force created when blood flows along the inner surface of endothelial cells.

It is determined by blood flow rate, viscosity, and vessel radius.
When shear stress increases (such as during exercise), it deflects the endothelial glycocalyx and activates signaling pathways.
This leads to nitric oxide (NO) release, causing vasodilation and helping regulate blood flow and blood pressure.

17
Q

What is the endothelial glycocalyx, and what role does it play in blood vessels?

A

The glycocalyx is a hair‑like, sugar‑rich layer that coats the inside surface of endothelial cells.
It is made of glycoproteins, proteoglycans, and sugar polymers that extend into the bloodstream.
Blood flow pulls on the glycocalyx, allowing it to act as a mechanoreceptor—detecting shear stress.
When stimulated, it sends signals that help trigger nitric oxide (NO) release, leading to vasodilation.

18
Q

What happens to endothelial cells when exercise increases blood flow, and how does this lead to vasodilation?

A

During exercise, blood flow increases, which raises shear stress on the endothelial surface.
The glycocalyx senses this mechanical force and activates signaling inside endothelial cells.
This signaling triggers nitric oxide (NO) release from the endothelial cell.
NO diffuses to smooth muscle and causes vasodilation, increasing blood flow to active tissues.

19
Q

How does acetylcholine (ACh) cause endothelial‑dependent vasodilation?

A

ACh binds to receptors on endothelial cells, not on the smooth muscle..
This activates intracellular signaling that raises Ca²⁺ levels in the endothelial cell..
Increased Ca²⁺ activates eNOS, which produces nitric oxide (NO).
NO diffuses into smooth muscle, causing relaxation and vasodilation.
If the endothelium is damaged, ACh cannot trigger NO release → ACh may cause vasoconstriction instead.