Flashcards in Cardiovascular control 2 Deck (18):
How to work out stroke volume, cardiac output and blood pressure?
Stroke volume = End-diastolic volume -End-systolic volume
Cardiac output= Stroke volume x Heart rate
Blood pressure = Cardiac output x Total peripheral resistance
what is the venous volume distribution affected by?
- peripheral venous tone (how constricted the vessels are).
-skeletal muscle pump
What are the ways of regulating blood flow?
There are intrinsic and extrinsic.
Autoregulation ( blood vessels change diameter in response to flow): is the intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance i.e. when the perfusion pressure drops, instead of the flow decreasing, the autoregulation causes the resistance to drop, so the flow increases/maintained.
What 2 possible theories are there for the compensatory mechanism of autoregulation?
1. Myogenic theory states that smooth muscle fibres respond to tension in the vessel wall (e.g. as pressure rises, fibres contract; stretch sensitive channels involved which allows calcium to go inside)
*sensor is fibre tension
2. Metabolic theory (as blood flow decreases, metabolites accumulate and and vessels dilate; subsequent increased flow ‘washes’ metabolites away)
*sensor is metabolite accumulation.
what happens if a vessel in injured, what is the mechanism for the autoregulation?
if a vessel in injured, you will get clots and platelets forming which release serotonin and cause constriction.
How do local hormones regulate blood flow?
Local ( endothelium derived):
-Nitric oxide (NO): potent vasodilator produced from arginine. NO diffuses into vascular smooth muscle cells
-Prostacylin: cardioprotective vasodilator synthesised from prostaglandin precursor (PGH2) – also has antiplatelet and anticoagulant effects
-Thromboxane A2 (TXA2): vasoconstrictor synthesised from prostaglandin precursor (PGH2) – also heavily synthesized in platelets (amplify platelet activation)
-Endothelins (ET): vasoconstrictors generated from the nucleus of endothelial cells – has minor vasodilator effects but principally a vasoconstrictor
How do circulating hormones control blood flow?
--Kinins: hormones that bind to receptors on endothelial cells and stimulate NO synthesis – vasodilator effects
--Atrial natriuretic peptide (ANP): secreted from the atria in response to stretch – vasodilator effects to reduce BP
--Vasopressin (ADH): secreted from posterior pituitary in response to high blood osmolality. Binds to V1 receptors on smooth muscle to cause vasoconstriction
--Noradrenaline/Adrenaline: secreted from adrenal gland and causes vasoconstriction
--Angiotensin II: potent vasoconstrictor product from the renin-angiotensin-aldosterone axis. Also stimulates SNS activity and ADH secretion
Where do the sympathetic and parasympathetic arise from and what is the main role of both?
Parasympathetic: arise from the cranial part of the spinal cord and the sacral part.
*important in controlling heart rate.
Sympathetic: Arising from thoracic vertebra and from the lumbar vertebra.
* important for controlling circulation and radius of vessels.
Explain the effects of noradrenaline?
Released by the sympathetic side.
Noradrenaline is released, will bind to alpha 1 adrenoreceptors to cause smooth muscle contraction and vasoconstriction.
How does the sympathetic nervous system effect blood vessels?
-All Blood vessels receive SNS post-ganglionic innervation Neurotransmitter = noradrenaline (NA)
-Always some level of tonic activity which can be moderated by having more or less tonic activity to cause Increased – causing vasoconstriction
Decreased – causing vasodilation
but we start of with some baseline of tonic activity.
There is no parasympathetic innovation to the blood vessels.
How do sympathetic influence the force of contraction?
-Noradrenaline binds to beta 1 receptors on the heart ( alpha 1 receptors on smooth muscle).
- causes increased cAMP
- increases protein kinase A
- this will phosphorylate the calcium release channel, the L-type channel and will have a positive effect on the calcium ATPase that takes up calcium back up.
-Ca2+ uptake into intracellular stores increased
-Ca2+ release from intracellular stores increased
- this therefore increases the calcium delivered to the myosin and therefore increase the contraction.
How do we control stroke volume?
- increase venous return which will increase EDV, increase stretch and increase cardiac output.
-Increase Sympathetic Nervous System activity to the heart which will increase the force of contraction.
-- increase plasma adrenaline
-bind to beta 1 receptor on the heart and increase force of contraction
How to increase cardiac output?
-increase plasma adrenaline
-increase Sympathetic Nervous System activity to the heart
-increase respiratory movements
Explain the anatomy of the baroreceptors?
There is the Target blood Pressure and the cardiovascular control centre which is the comparator. This sends signal to the autonomic nervous system and evoke to release noradrenaline etc. This causes vasoconstriction or vasodilation, which causes a new blood pressure. This is seen by the baroreceptors.
These are the sensors that feed back to the cardiovascular control centre/ vasomotor centre.
Baroreceptors are located carotid bodies:
- send afferent pulses back down the Glossopharyngeal nerve
-send afferent pulses down the vagus nerve
-and then the vagus nerve carries efferent to the SAN ( 2 way system)
What do baroreceptors respond to?
More stretch causes more firing.
Baroreceptors respond to changes in arterial pressure
Explain the mechanism of what happens when the baroreceptors stretch
-Stimulates the parasympathetic nerves to heart.
-at the same time, it inhibits sympathetic innervation to heart, arterioles and veins.
-The Sympathetic nerve contains inhibitory inteneuron which inhibits tonic activity that comes down the sympathetic nerve
Most blood vessels receive sympathetic post-ganglionic innervation where the transmitter is?