Cardiovascular System Flashcards
Type od blond vessels
- Elastic conducting arteries
- Muscular distributing arteries
- Arterioles
- Capillaries
- Venules
- Veins
Layers of blood vessels
> Tunica Intima innermost
> Tunica Media middle
> Tunica adventitia or externa outer)
Tunica intima(innermost)
-Thin, single layer - tight unctions to prevent leaks, releases vasoactive substances
Tunica media (middle)
-Smooth muscle + connective tissue elastin
collagen adds to the strength of the vessels
-Contains internalexternal elastic lamina
-sympathetic innervation
-important for blood pressure control
Tunica adventitia/externa (outer most)t
-Connective tissue (collagen + elastin)
-contains nerves, moroplasts, adipocytes
-control of overexpansion collapse
-vasa-vasorum in some large vessel
Characteristics of a vein
-fairly thin outer wall
-thin layer of muscle and elastic fibres
-large lumen
Difference between an artery and a vein
-an artery has a thicker outer wall with a thick layer of muscle as well as smaller lumen
Characteristics layers of the artery
-thick outer wall
-Thick layer of muscles and elastic fibres
-small lumen
Characteristics/layers of a capillary
-wall made of a single layer of cell( endothelium)
-very small lumen
Large arteries
-are elastic eg aorta
-absorb pressure generated by cardiac contractions to reduce peak systolic pressure and ensure better flow
-narrow lumen but thick muscular walls(dilate or constrict in a regulated manner to regulate and help direct blood flow to activate organs)
Small arteries/arterioles
-small and act as a resistance vessel
-limited elasticity but do contain smooth muscle
-regulate blood pressure and flow through capillaries
-diameter is regulated by many mediators released by the inner lining endothelial cells
Vasodilators
Histamine
Nitric oxide
Prostaglandins
Bradykinin
Adenosine
Vasoconstrictors
Endothelium,
thromboxane,
noradrenaline
Adrenaline
Venules
-narrow diameter and no tunica media
Medium diameter vein
-thin tunica media with few smooth muscle cells
Larger diameter veins
-Thicker tunica externa,relatively thick tunica media
-larger veins also contain valves to assist the one way flow of blood back to the heart (muscle contractions Aida venous return,varicose veins from in valves)
How is tissue blood flow controlled
-controlled by vasoconstriction or dilation of small arteries/arterioles supplying the tissue
-arterioles and their pre-capillary sphincters control the blood flow
-smooth muscle contraction/relaxation precapillary sphincters is regulated by a range of local(metabolic) and extrinsic(neural( mechanisms
What’s a precapillary sphincters
Segments of smooth muscle that help direct blood flow into capillaries
Types of capillaries
Continuous
Fenestarted
Discontinuous
Capillaries
-single cell layer
-no tunica media or externa
-controls fluid movement
-Site of gas diffusion
-respond to vasoactive growth factors,mediators and cytokines
-stimulate blood clotting
-participate on angiogenesis
Continuous capillary
Most common type
Fenestrated capillary
Permeable/Leaky eg renal
Discontinuous capillary
Capillaries dorm sinusoids in liver/spleen/bone
% difference between venous return and cardiac output
Venous return is 80%
Cardiac output is 20%
What do arteriole provide
-blood to many capillaries
-flow is slow allowing better gas and nutrient exchange
-as blood flows through capillaries there is a net loss of fluid to interstitial fluid leading to a fall in blood pressure
-plasma proteins generate osmotic pressure(these fluids form urine in the kidney and lymph elsewhere
Lympathic vessels
-plasma like lymph is derived from fluids that leak from the arterial ends on capillaries due to blood pressure
-Lymph capillaries are found in all tissues except the CNS, bone marrow and epidermis
-Fluid enter tiny lymph capillaries and is returned to blood to prevent edema and help maintain normal blood volume and pressure
-Lymphatic fluid contains white blood cells
but no red cells
-Lymph flows, via lymph nodes, to the subclavian vein. Valves in the larger lymphatic vessels prevent back flow
Myogenic tone (influences on VSM(vascular smooth muscle )in vivo)
• Neuronal
>Sympathetic noradrenergic (a1 and B2)
• Local
>Myogenic tone (ABP)
>Endothelium derived substances
Vasodilators: e.g., nitric oxide, prostacyclin Vasoconstrictors: endothelin, thromboxane
>Substances released from the surrounding tissue / cells
Vasodilators: e.g., ATP, ADP, AMP, adenosine
• Hormones
• Adrenaline, Acetylcholine, Histamine, Angiotensin
• Intracellular free calcium
• External factors like muscles squeezing blood vessels
Myogenic tone smooth muscle contraction
• Increase in intracellular Ca2+ concentrations initiates contraction
• Ca2+combines with acid protein
“calmodulin”
• Ca2+/Cal complex activates Myosin Light
Chain Kinase -> phosporalates 20 kDA light chain of myosin
• Interaction of myosin with actin
• Highly regulated process
• Maintenance of smooth muscle tone
• Myosin Light Chain Phosphatase reverses the biding of myosin with actin -> smooth muscle relaxation
Endothelin
• The most potent vasoconstrictor substance discovered (peptide)
•Formed from Big ET in endothelial cells - cleaved by ET converting
enzyme (ECE).
Triggered by agonists (noradren, thrombin, AVP) which stimulate receptor.+ hypoxia or ischaemia
Three isoforms: ET-1, ET-2, ET-3
Stimulated by:
Endotoxin, various cytokines and growth factors, adrenaline, hypoxia, low shear
stress
Inhibited by:
NO, PGE2, PGI2, high shear stress
Endothelin binds to two receptors ET and ET
G-protein coupled
ET Expressed on vsmc -> vasoconstriction
•ET, -receptor antagonist used in treating pulmonary hypertension
Angiotensin II
Highly potent vasoconstrictor
•Constricts cutaneous, splanchnic and renal vasculature
• Renin acts on angiotensinogen -Yang I
• ACE converts ang I -> ang lI
• Ang Il actions are mediated mainly via
All receptors
CA2+ and vascular relaxation
Dilation induced by cAMP/cGMP (2nd messengers)
CAMP (cyclic adenosine mono phosphate) stimulated PKA - opens K”ATP channels
• cGMP (cyclic guanosine mono phosphate) stimulates PKG - opens K’ArP and K’caz+
• Therefore, both inhibit Ca?* influx via VOCCs
• They also,
Stimulate SERCA (SR)
Stimulate PMCA (plasma membrane)
• Reduce sensitivitv or contractile apparatus
MLC P sensitivity > less force
& MLC K
• Because cAMP + CGMP stimulate PKG which inhibits cross-bridge formation
So, CAMP and cGMP act in synergistic ways
NB, NO is the main stimulus for cMP
Whereas a range of agonists act via cAMP (PGIz, adrenaline via B2)
Vascular endothelium-first evidence
•solated artery in organ bath
arranged for recording tension in wall (level of contraction in VSM)
Pre-constricted with
Phenylephrine (PE)
• Ach sometimes evokes relaxation sometimes but causes constriction at other times
Types of blood pressure
-systolic
-diastolic
-mean blood pressure
-pulse pressure
Systolic pressure
blood pressure is the pressure when the ventricles (bottom chambers of heart) contract to eject blood forward. For systemic circulation this is the pressure generated by the left ventricle.
Diastolic pressure
blood pressure is the pressure on the blood vessels when the heart muscle relaxes.
Mean blood pressure
is calculated in multiple ways. Most common calculation used is the sum of two-third of diastolic and one-third of systolic pressure. Another common calculation used is diastolic pressure + one-third of pulse pressure
Pulse pressure
difference between systolic and diastolic blood pressure.
Systemic circulation
Left Ventricle pumps at a higher pressure
(80 - 120 mmHg). Above 140 mmHg at rest
is abnormal
Pulmonary circulation
Right ventricle pumps blood at a lower pressure 8 - 20 mmHg) to lungs. Above 25 mmHe at rest is abnormal.
Use of blood pressure
Blood pressure is the driving force for blood flow
Pressures decrease throughout the vascular system:
~Arteries > Arterioles > Capillaries > Venules > Veins
Poiseuille’s law
Flow is proportional o the pressure divided by the resistance to flow
~if pressure gradients reduce the flow reduces
~if resistance increases the flow will reduce
List regulators of blood pressure
.Cardiac outout Heartrate and stroke volume
2. Total perioneral resistance
List regulators of blood pressure
o. Renin•on protensin didosterone system
4. Antidiuretic hormone ADHE Vasopressin
5. Natriuretic peptides TANP
6. Baroreflex
7. Other factors (metaboretlex, mechanoretlex, chemoretlex, central commano, pain, temperature, gravity…
Regulators of blood pressure:heart
Pressure generated by the heart
and its cardiac outour are the main sources of blood pressure
Cardiac output (heartrate × stroke
Stroke volume is affected oy the size of the heart and also ov the
force o cardiac contraction(inotropy)
Regulators of blood pressure :blood vessels
Flow is proportional to the pressure gradient divided by the resistance to flow (Poiseuille’sLaw):
-if pressure gradients reduce the flow reduces ~if resistance increases the flow will reduce
Resistance is altered by changing the diameter of the
vessels:
~vasodilation:
†diameter, resistance; blood flow
-vasoconstriction: diameter, resistance; blood flow
Small arteries / arterioles are the most important resistance vessels
Homeostatic regulation of blood pressure
No single set point for blood pressure repulation
Diuresis: production of urine, extraction of volume
Natriuresis:excretion of sodium in urine
Regulators of blood pressure :renin-angiotensin aldosterone system
Renin: is a proteolytic enzyme secreted by kidneys in response to fall in sodium, acts on angiotensinogen to produce angiotensin 1
Angiotensin 1 (an inactive peptide) which with the help of angiotensin converting enzyme converts angiotensin 1 to angiotensin 2 (active form) in lungs
Angiotensin 2 is a potent vasoconstrictor.
Systemic circulation
Kidneys
Angiotensin 2 also leads to the production on aldosterone from adrenal cortex which increases reabsorption of salt and water from distal tubules (increased volume).
Regulators of blood pressure:antidiuretic hormone(vasopressin)
-released from posterior pituitary in response to decreased volume and reduced blood pressure
-generally;vasoconstrictors in the body particularly skin and splanchnic circulation
-brain and the heart :vasodilator actions
-also leads to bradycardia(slows heart rate)
Regulators of blood pressure:antidiuretic hormone(vasopressin)
In Kidneys:
Reabsorbs water from the final third of the distal tubules and collecting ducts through increased permeability»_space;» increase in blood volume»_space;» decrease in urine output
+
Increased sodium reabsorption»_space;» increases osmotic pressure gradient
»» fluid retention»_space;» concentrated urine with low volume
Regulators of blood pressure:natriuretic peptides
ANP: atrial natriuretic peptide is a short-lived peptide, released from atrial myocytes in response to increased pressures within the atria.
Venous Pressures
BNP: brain natriuretic peptide is also a short-lived peptide, released from ventricular myocytes (mainly left ventricle) in response to increased pressures within the
ventricles
How do natriuretic peptides work
Their actions inhibit renin and reduce angiotensin 2 concentrations to inhibit vasoconstriction.
They also inhibit aldosterone and promote salt and water uresis (reduced volume)
They also directly cause some vasodilation.
^ cGMP
^ NO (vasodilator)
~ sympathetic tone
< noradrenaline
What type of enzyme się renin
Proteolytic
Baroreflex
-Baro receptors sense pressure within arteries
-increased pressure stimulates barorerceptors to increase their activity
-decline in pressure reduces Baro receptor activity
Hypertension
-increased Baro receptor activity
-decreased sympathetic drive
-increased parasympathetic drive
Hypotension
-decreased Baro receptor activity
-decreased parasympathetic drive
-increased sympathetic drive
Are Baro receptors set-points fixed
Short term acute regulators not long teem controllers of blood pressure
What happens to blood pressure at night
-slows down(dips)
What happens to bloood poressure as you get older
It increases due to the arteries getting stiffer
Effect of vasoconstriction
Increase in blood pressure
Effect of vasodilation
Decrease in blood pressure
Auto regulation
-Intrinsic ability of an organ to maintain a constant blood floe despite changes in blood pressure
-auto regulation of flow through blood vessels ,particularly arterioles occurs in response to changes in blood pressure
-its important in the brain ,Heart and kidney
-it is mediated by metabolic products eg co2 along side extrinsic factors like neutral tone to the blood vessels that regulate flow via vasodilation like active hyperaemia
-it also promotes vasoconstriction when flow is fast due to the removal of local controls such as co2
Neutral factors that control blood pressure/heart rate
-pain
-temperature
-gravity
-pulmonary stretch
Central command
-chemoreception
-skeletal muscle/proprioception
-sympathetic alpha receptor activation causes vasoconstriction and beta2 receptors activation lead to vasodilation in muscles
-stretch of the heart(force generated) detected :volume and pressure receptors
-vagal fibres that innervate the heart
-sympathetic or parasympathetic system activation that adjusts Heart rate
