10 Regulation of the Cardiovascular System Flashcards
Q: What are veins considered? What do they have? What does central venous pressure determine?
A: storage vessels for blood volume - they have capacitance
the amount of blood flowing back to the heart
Q: What is venous volume distribution affected by? (4)
A: -Peripheral Venous Tone
- Gravity
- Skeletal Muscle Pump
- Breathing
Q: What does venous return to the heart determine? (2) according to?
A: stroke volume- Starling’s law
the amount of stretch and hence determines the force of contraction
Q: What do the arterioles determine? How?
A: -flow control (main control)
-varying constriction by altering vessel radius
Q: What determines the extent of constriction? What does constriction determine?
A: the pattern of organisation of innervation to particular vascular beds i.e. the number of adrenoreceptors will affect the blood flow to an organ
-determines compliance and hence venous return
Q: What are the 3 ways of regulating flow? Summarise.
A: Local Mechanisms
-Intrinsic to the smooth muscle itself or closely associated
Hormonal
-Circulating hormones
Autonomic Nervous System
-Innervates arterioles and veins to produce constriction or dilation
Q: What do local mechanisms to regulate blood flow involve? define. Describe how this works when blood pressure drops. Draw a graph to show what happens without this mechanism.
A: autoregulation= the intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance
there will be a gradual decrease in resistance and hence a gradual increase in flow
REFER 2 graphs- one for resistance and one for flow
Q: What are the 2 theories behind the mechanism of ‘autoregulation’ to regulate blood flow?
A: Myogenic Theory = smooth muscle fibres respond to stretch (stress operated ion channels) - as pressure rises, the muscle fibres start contracting to keep flow constant
Metabolic Theory = if the vessels supplying a particular vascular bed contract, the flow to the vascular bed decreases and the vascular bed produces MORE METABOLITES - as more metabolites are produced, it feeds back on the vessel that’s supplying the bed and causes vasodilation and hence allows more flow to the vascular bed and the metabolites which triggered this response are washed away
Q: How can autoregulation be changed?
A: by injury to the vessel - when a vessel is injured, platelets aggregate and they release serotonin which is a powerful vasoconstrictor which will constrict the injured vessel
Q: In local mechanisms that regulate flow, what else is involved? 4 examples.
A: Substances released from the endothelium
Nitric Oxide - plays a key role in vasodilation
Prostacyclin + Thromboxane A2 (vasodilator and vasoconstrictor respectively)
Endothelins - potent vasoconstrictors
Q: Which 3 substances are involved in the systematic regulation of blood flow by hormones? 1-interactions with? tend to? 2- secreted from? cause?
A: Kinins
- Have complex interactions with the Renin-Angiotensin System
- Tend to relax vascular smooth muscle
ANP (Atrial Natriuretic Peptide)
- Circulating peptides that are secreted from the cardiac atria
- As the atria stretch they release more ANP which causes vasodilation
Circulating Vasoconstrictors
Q: Name 3 circulating vasoconstricters.
A: -Vasopressin
- Angiotensin II
- Noradrenaline
Q: What do parasympathetic nerves consist of? (3)
A: LONG preganglionic fibre and a short postganglionic fibre - the parasympathetic ganglion will be right beside the sinoatrial node
Q: Why are the parasympathetic and sympathetic systems important? (2)
A: Sympathetic - generally controls the FLOW
Parasympathetic - important in regulating HEART RATE
Q: What do sympathetic nerve fibres innervate? Distribution? What does this mean?
A: ALL VESSELS EXCEPT CAPILLARIES (and precapillary sphincters and some metarterioles)
Distribution of sympathetic nerve fibres is NOT even - more sympathetic nerve fibres innervate vessels supplying the kidney, gut, spleen and skin and fewer innervate the skeletal muscle and the brain
there is more potential to constrict the blood going to these places so that we can divert blood to the organs that we need more
Q: What is the relationship between circulating adrenaline and smooth muscle? causes? What can adrenaline bind to at high concentrations? result?
A: Circulating adrenaline binds with high affinity to smooth muscle beta-2-adrenoreceptors to cause vasodilation in some organs, however the effect is very concentration-dependent
At high concentrations, adrenaline can bind to ALPHA adrenoreceptors which can override the vasodilatory effects of the beta-2-adrenoreceptor stimulation and produce vasoconstriction
Q: The constriction you see in blood vessels is the effect of which receptors?
A: alpha-1-adrenoreceptor
Q: Where is the vasomotor centre VMC located? What does it consist of? (3) What does it allow in terms of exercise? due to?
A: bilaterally in the reticular substance of the medulla and the lower third of the pons
- Vasoconstrictor Area (Pressor)
- Vasodilator Area (Depressor)
- Cardioregulatory Inhibitory Area
anticipatory response to exercise - your heart rate and ventilation rate will go up slightly before exercise because of these higher sensors in the brain
Q: What can exert excitatory and inhibitory effects on the VMC? What do the lateral portions of the VMC control? how? (2) What do the medial portions control?
A: (vasomotor centre)
Higher centres in the brain (such as the hypothalamus)
heart activity by influencing heart rate and contractility
transmits signals via the vagus nerve to the heart that tends to decrease heart rate
Q: What do blood vessels receive in terms of the nervous system? Which neurotransmitter is involved? What is there always? At baseline?
A: sympathetic postganglionic innervation
NORADRENALINE
- some tonic activity
- there is a certain frequency of the impulses which maintains vasomotor tone
Q: What happens if you increase nerve traffic to blood vessels? Decrease? What is there not much of in the vascular system?
A: constrict the vessel
dilate the vessel
There is NOT much parasympathetic innervation of the vascular system
Q: Which 3 areas control the vessel radius?
A: -Local Controls (Autoregulation)
- Circulating Hormones
- Sympathetic Vasoconstrictor Nerves
Q: In terms of cardiac innervation, how can we change heart rate? What part of the heart receive innervation? which kind? What is normal resting heart rate? With no innervation?
What damage can be done so we lose the ability to increase heart rate? result?
A: by dual innervation - sympathetic and parasympathetic
sinoatrial nodal cells receive sympathetic and parasympathetic innervation
70, 100bpm
cut the sympathetic nerves and heart rate falls
Q: What slows down heart rate? how? What increases heart rate? how?
A: Parasympathetic slows heart rate down because acetylcholine decreases the gradient of the pacemaker potential - this means that the potential takes longer to reach threshold and fire
Sympathetic increases heart rate because adrenaline and noradrenaline increases the gradient of the pacemaker potential so threshold is reached more quickly
Q: By which law can force of contraction be increased? What kind of activity can increase the force of contraction? what can it control as a result? What can’t change the force of contraction?
A: Starling’s
- sympathetic
- heart rate
parasympathetic activity
Q: What are the 2 ways noradrenaline increases heart contraction?
A: -Noradrenaline binds to Adrenoreceptors (eg beta 1) which increases the amount of cAMP which activates PKA which phosphorylates the L-type calcium channels and the SR calcium release channel and SERCA => get MORE CALCIUM INFLUX and more calcium taken back up into the stores
can also act on beta-1-receptors in heart
Q: What can stroke volume be increased by? (2)
A: Increased Sympathetic Activity
Plasma Adrenaline
Q: Describe intrinsic control of stroke volume. What else can affect this? (2)
A: venous return which sets the end-diastolic volume (stretch) which increases the force of contraction
- can get more blood back to the heart (increase venous return) if we increase respiratory movements
- decreasing intrathoracic pressure helps the filling of the heart
Q: What can we get rapid changes in as part of the fight or flight response? (3)
A: RESPIRATORY MOVEMENT
PLASMA ADRENALINE
INCREASE SYMPATHETIC ACTIVITY
Q: Where are baroreceptors? (2) What do they do? What are they?
A: aortic arch and in the carotid sinus (carotid bodies)
Baroreceptors in the carotid bodies feedback to the vasomotor centre via the glossopharyngeal nerve
The aortic arch baroreceptors feedback to the vasomotor centre via the vagus nerve
feedback nerves to the VMC
Q: What are the 2 feedback nerves to the VMC?
A: (vasomotor)
Aortic Arch Baroreceptor = Vagus Nerve
Carotid Sinus Baroreceptors = Glossopharyngeal Nerve
Q: Between which pressures do carotid sinus baroreceptors respond to? Between which pressures is the baroreceptor reflex most sensitive?
A: 60 and 80 mmHg
90-100mmHg
Q: How do baroreceptors respond to an increase in pressure? result? (2)
A: fires more
Increase in baroreceptor firing = Increase in in parasympathetic activity AND DECREASE in sympathetic activity
Q: Draw the reciprocal innervation diagram.
A: REFER
Q: What connects sympathetic nerves? what do these structures do?
A: via a series of inhibitory interneurones which slows down the tonic activity
Q: Parasympathetic stimulation of the heart occurs via? causes? What does parasympathetic activity reflect?
A: vagus nerve, decreased heart rate
exactly what happens in terms of baroreceptor activity
Q: What does a decrease in sympathetic stimulation to the heart cause? (2) to the blood vessels?
A: decreased heart rate and stroke volume
vasodilation
Q: What does nerve activity from the baroreceptors reflect? What results in increased blood pressure? fed back? triggers? Result?
A: rise or fall in pressure
huge increase in firing activity from the baroreceptor
increase in baroreceptor firing -> fed back to the vasomotor centre = triggers increased traffic in the vagus nerve
= brings about a decrease in heart rate
Q: What does an increase in parasympathetic activity cause?
A: an increase in acetylcholine production in the SAN which decreases the gradient of the pacemaker potential and causes a decrease in heart rate
Q: What does less innervation from sympathetic nerves lead to in terms of the heart? vessels? Overall result?
A: decrease in the force of contraction
increase in vessel radius
DECREASE IN BLOOD PRESSURE
Q: What’s the equation for mean systemic arterial pressure?
A: Cardiac Output x Total Peripheral Resistance
