CVS 10 - Regulation of CVS Flashcards
Veins store blood volume (they have capacitance). What 4 factors affect venous volume distribution?
- Peripheral venous tone
- Gravity
- Skeletal muscle pump
- Breathing
What does central venous pressure determine?
Amount of blood flowing back to the heart, which determines stroke volume
What are the 3 ways of regulating flow?
- Local mechanisms
- Hormonal mechanisms
- Autonomic nervous system
Compare and contrast myogenic theory and metabolic theory.
Both theories try to explain why there is a decrease in R when P drops, which increases F.
Myogenic: VSMC respond to stretch. As P increases, muscle fibres contract to keep flow constant
Metabolic: If vessels supplying a vascular bed contract, F decreases and so the vascular bed produces more metabolites that cause vasodilation. This allows greater flow to the vascular bed.
How can autoregulation be changed?
If a vessel becomes injured. Platelets aggregate around injured vessels and release serotonin (a powerful vasoconstrictor)
Give 3 ways in which systemic blood flow is regulated.
- Kinins - interact with RAS and relax VSMC
- ANP (Atrial Natriuretic Peptide) -peptides secreted from atria. Atria stretching causes more ANP release causing vasodilation.
- Circulating vasoconstrictors - vasopressin/Ang 2/NA
Difference in structure between sympathetic and parasympathetic neurone?
Parasympathetic Neurone = long preganglionic neurone, short post ganglionic neurone.
(sympathetic is the other way round)
In the autonomic NS, which aspect of heart does sympathetic control? Which part does parasympathetic control?
- Sympathetic = controls flow
2. Parasympathetic = regulates HR
Which vessels do sympathetic nerve fibres innervate?
All vessels except capillaries.
Describe the distribution of sympathetic nerve fibres. Why is this important?
More sympathetic innervation to vessels supplying Kidneys, Gut, Spleen, Skin.
That way, NA (which binds more preferentially to a1-receptors) cause SM contraction and vasoconstriction.
Describe the concentration dependent nature of adrenaline.
Adrenaline binds with high affinity to b2-adrenoreceptors and cause vasodilation.
At high concentrations however, adrenaline can bind to a-adrenoreceptors and cause vasoconstriction (overriding the vasodilatory effects of b2-adrenoreceptor stimulation).
Which receptor is activated when blood vessels constrict?
a1-adrenoreceptor
Where is the Vasomotor Centre (VMC) located?
Located bilaterally in the medulla and pons.
It transmits impulses via the spinal cord to almost all blood vessels
What are the 3 parts of the VMC.
- Vasoconstrictor Area (pressor)
- Vasodilator (depressor)
- Cardioregulatory Inhibitory Area
What can higher centres in the brain do?
They can exert excitatory/inhibitory effects on VMC.
They allow an anticipatory response to exercise - HR and VR increases slightly before exercise due to this
What do the lateral portions of the VMC generally control?
Controls HR and Contractility
What do the medial portions of the VMC control?
They transmit signals via Vagus nerve to the heart - tends to decrease HR.
How is blood vessel diameter nervously controlled?
- Blood vessels receive sympathetic postganglionic innervation (through NA)
- Baseline frequency of impulses maintains Vasomotor tone.
- Increasing nerve traffic = vasoconstriction
- Decreasing nerve traffic = vasodilation
- Very little parasympathetic innervation of vascular system.
Which 3 areas allow control of blood vessel radius?
- Local controls (auto regulation)
- Circulating hormones
- Sympathetic vasoconstrictor nerves
Heart rate (cardiac innervation) is influenced by dual innervation - sympathetic and parasympathetic. How does parasympathetic work? How does Ach work?
Parasympathetic slows HR down - Ach decreases gradient of pacemaker potential, meaning potential takes longer to reach threshold and fire.
Sympathetic increases HR - A and NA increases gradient of pacemaker potential.
How is force of contraction controlled (other than Starlings Law).
(CONTRACTILITY CANNOT BE CHANGED BY PARASYMPATHETIC ACTIVITY)
- NA binds to b1-adrenoreceptors.
- cAMP levels increased. cAMP activated PKA, which phosphorylates L-type Ca channels and SR Ca release Channel and SERCA.
- Therefore, more Ca influx , and more Ca uptake into stores.
- Overall, force of contraction increased.
How can SV be increased?
- Increase sympathetic activity (extrinsic)
- Increase plasma adrenaline
- Increase EDV - by increasing venous return, increase atrial pressure and decreasing intrathoracic pressure (e.g. increasing respiratory movements)
What does the fight or flight response affect?
- Respiratory movement
- Plasma adrenaline
- Increased sympathetic activity
How do the Aortic Arch baroreceptor and the Carotid sinus baroreceptor feed back to the VMC?
Aortic Arch Baroreceptor = Vagus Nerve
Carotid Sinus Baroreceptor = Glossopharyngeal nerve
What do baroreceptors do?
At what pressures are the baroreceptor reflexes most sensitive?
They respond to changes in pressure
Baroreceptor reflex most sensitive around 90-100mmHg.
Explain how baroreceptors can cause a decrease in HR if pressure increases.
- Receptor fires more via afferent (vagus) nerve. Increases parasympathetic activity.
INCREASE BARORECEPTOR FIRING = INCREASED PARASYMPATHETIC ACTIVITY
- Simultaneously, inhibitory interneurones are activated which slow down sympathetic activity. (This also causes vasodilation)
Increased baroreceptor firing = decreased sympathetic activity
Where does parasympathetic stimulation of the heart come from?
Vagus nerve
MAP =?
MAP = CO x TPR