CV - Intrinsic and extrinsic control of blood vessels Flashcards
Describe need to control vessels and flow and the concept of vascular tone:
Need for control:
- vascular resistance controls local flow but also BP & CO
- vasomotor tone redistributes cardiac output to appropriate targets
- Ensures proper perfusion to organs based on metabolic demands
- Maintains systemic blood pressure and local tissue oxygenation
Concept of vascular tone:
- Baseline level of constriction in blood vessels due to constant sympathetic activity
- Vasomotor tone (resistance) is the sum of basal tone & any constrictor or dilator influences
- Regulated by intrinsic (local) and extrinsic (systemic) mechanisms
- Balances between vasodilation and vasoconstriction to match demand
describe sympathetic vasoconstrictor control:
sympathetic vasoconstrictor fibres innervate most blood vessels
most important in regulation of blood pressure sympathetic nerve activity causes release of neurotransmitters from postganglionic nerves
Noradrenaline (Norepinephrine) release from sympathetic nerves binds to α1-adrenergic receptors → smooth muscle contraction → vasoconstriction
Increased sympathetic activity = more vasoconstriction → increased blood pressure.
Decreased sympathetic activity = vasodilation → reduced resistance & blood pressure.
Effects:
- Critical for maintaining blood pressure during standing
- Redirects blood flow during exercise or hemorrhage
- Constriction of veins increases venous return → maintains cardiac output
Describe sympathetic innervation:
Most arteries, arterioles, and veins receive sympathetic innervation
High innervation in skin, splanchnic organs, kidneys for systemic blood pressure control
Low innervation in brain and heart (local metabolic control dominates).
Describe the adrenal medulla in relation to extrinsic vascular control:
Part of the sympathetic nervous system but acts via hormones
Releases adrenaline (epinephrine) & noradrenaline into circulation
α1-receptors → Vasoconstriction (gut, skin, kidneys)
β2-receptors → Vasodilation (skeletal muscle, heart, liver)
Fight or flight response - prioritises blood flow to heart, muscles and brain
Describe Sympathetic vasodilator control in relation to extrinsic vascular control:
Less common than vasoconstrictor control
a form of active skin vasodilatation that originates from sympathetic cholinergic innervation of sweat glands
cause vasodilation to aid in heat loss
Mediated by β2-adrenergic receptors (activated by adrenaline from adrenal medulla)
Describe Parasympathetic vasodilator control in relation to extrinsic vascular control:
Mainly affects salivary glands, GI tract, and erectile tissue
Acetylcholine (ACh) stimulates nitric oxide (NO) release from endothelium → vasodilation
Example:
. penile erection caused by nitridergic nerves
release NO (via nNOS)
increases cGMP
vasodilatation of corpus cavernosum & helicine arteries
similar mechanism in clitoris
Describe renin and angiotensin in relation to extrinsic vascular tone:
Actions of Angiotensin II:
Vasoconstriction: Angiotensin II is a potent vasoconstrictor, especially acting on AT1 receptors located on vascular smooth muscle, leading to increased systemic vascular resistance (SVR) and elevated blood pressure.
Aldosterone Secretion: Angiotensin II stimulates the adrenal cortex to release aldosterone, which increases sodium and water retention by the kidneys, thereby expanding blood volume and further increasing blood pressure.
Antidiuretic Hormone (ADH) Release: Angiotensin II also promotes the release of ADH from the posterior pituitary, further enhancing water retention by the kidneys.
Sympathetic Nervous System Activation: It enhances sympathetic activity, contributing to vasoconstriction and increased heart rate.
renin secretion controlled by:
- decreased renal artery pressure
- increased renal sympathetic nerve activity
- decreased Na+ load
Describe the myogenic response in relation to intrinsic control:
myogenic response refers to the ability of blood vessels to constrict or dilate in response to changes in intrinsic pressure (i.e., the stretch of vascular smooth muscle due to changes in blood pressure)
Mechanism:
- Increased intravascular pressure stretches the vascular smooth muscle
- VOCC’s open and intracellular Ca2+ increases
- triggers vascular constriction to maintain constant blood flow despite fluctuations in blood pressure
- Conversely, decreased intravascular pressure leads to vasodilation, which helps restore normal blood flow.
Importance:
Autoregulation - maintains tissue perfusion
Prevention of hyper fusion - prevents excessive pressure from damaging capillaries and tissues by limiting the increase in blood flow during hypertension
Describe the endothelium in relation to intrinsic control:
The endothelium provides important vasoactive signals to vascular smooth muscle. Blood flow in larger conduit arteries causes shear stress on the endothelium which then activates eNOS and releases NO
The NO quickly diffused across to the vascular smooth muscle and results in increase cGMP
This then phosphorylates and deactivates protein kinase and causes vasodilatation
this causes a drop in TPR and arterial BP which can be fatal.
In smaller arteries the shear stress causes vasodilatation caused by release of endothelial-derived hyperpolarising factor (EDHF)
The endothelium also tonically produces small amounts of the vasoconstrictor, endothelin. This makes a small contribution to TPR, as antagonists for endothelin cause a slight decrease in arterial BP
Describe Vasoactive metabolites in relation to intrinsic control:
Vasoactive metabolites are substances produced by tissues that influence vascular tone, typically in response to metabolic needs such as increased oxygen consumption or carbon dioxide production
Changes in chemical environment surrounding blood vessels causes increased blood flow to metabolically active regions like cardiac muscle, brain tissue
Adenosine - Released during conditions of low oxygen (hypoxia) and high carbon dioxide (hypercapnia as it promotes vasodilation
Lactate - promotes vasodilation, produced during anaerobic respiration
CO₂: Elevated carbon dioxide levels in tissues (such as during exercise) lead to vasodilation
H⁺ (Protons): An increase in H⁺ (acidosis) promotes vasodilation to improve the clearance of excess acids
K⁺: Increased levels of potassium (e.g., during muscle activity) contribute to vasodilation, helping to maintain proper blood flow during physical exertion
Describe autocoids in relation to intrinsic control:
Autocoids are locally released organic chemicals acting on nearby cells to regulate vascular tone and other physiological processes
often released as part of inflammatory response, released by platelets, mast cells, white blood cells
typically act in a paracrine manner, meaning they influence nearby cells or tissues without entering the bloodstream, ensuring localized control of vascular tone
Key autocoids:
Bradykinin - vasodilator that increases vascular permeability and induces smooth muscle relaxation
Prostacyclin (PGI₂): Produced by the endothelium, prostacyclin promotes vasodilation and inhibits platelet aggregation
Nitric Oxide (NO): A key vasodilator, nitric oxide is produced by endothelial cells in response to shear stress or certain signaling molecules
Endothelin: A potent vasoconstrictor produced by endothelial cells, endothelin works via ET receptors to raise vascular tone and blood pressure
Describe temperature in relation to intrinsic control:
decreased temperature leads to increased α2-binding which causes greater vasoconstriction, especially cutaneous vessels
decreased temperature below 10˚C blocks nerves causes vasodilatation protecting tissue from damage
Heat induced vasodilation:
- When tissue temperature increases, blood vessels dilate to facilitate heat dissipation
- Heat relaxes vascular smooth muscle, leading to vasodilation
- enhances the activity of potassium (K⁺) channels, leading to hyperpolarization of smooth muscle cells and reduced contraction
- Higher temperatures upregulate HSPs, which protect endothelial function and contribute to vasodilation
Cold induced vasoconstriction:
- When temperature decreases, blood vessels constrict to preserve core body temperature
- causes vascular smooth muscle constriction
- Cold exposure enhances sympathetic activity, increasing norepinephrine (NE) release, which binds to α1-adrenergic receptors, promoting vasoconstriction
Describe the neuroeffector junction:
Postganglionic nerve branch as they reach the adventitia and knobbly varicosities are apparent that contain transmitter-filled vesicles.
The branches permeate the outer layers of smooth muscle.
There are no specializations like the NMJ of skeletal muscle that have Ach receptors congregated below the motor end plate.
Instead, adrenergic (and other transmitter) receptors are distributed all over the smooth muscle so when transmitter is released it diffuses and interacts with receptors all around the varicosities (intra- and extra-junctional receptors),
