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Discuss the roles of parasympathetic and sympathetic systems in control of
blood pressure
INTRO
Parasympathetic nervous system (PNS) and sympathetic nervous system (SNS)
are divisions of the autonomic nervous system that are involved in the control of
blood pressure. It is important to control arterial blood pressure to keep it inside
a certain range, as hypotension will result in not enough oxygenated blood
reaching tissues to provide oxygen for respiration, while hypertension can
damage fragile circulations such as the pulmonary capillary beds. The PNS and
SNS, using information from baroreceptors to determine whether the blood
pressure is too high or too low, control blood pressure by altering cardiac output
and vascular resistance, since Blood pressure= cardiac output x vascular
resistance.
EFFECT ON THE HEART
Sympathetic nerve fibres increase blood pressure by causing an increased heart
rate and increasing the force of contraction of the heart muscle, while
parasympathetic nerve fibres have the opposite effect. Increased heart rate and
contraction force result in a greater cardiac output, as it is determined by the
heart rate itself, and the amount of blood pumped out of each ventricle per beat,
the stroke volume; which is increased by an increased force of contraction.
Cardiac output= stroke volume x heart rate. The heart is innervated with
parasympathetic and sympathetic nerve fibres. Both branches of the autonomic
nervous system originate in the cardiovascular centre of the brain, but reach the
heart via different pathways. The sympathetic fibres extend from the spinal cord
in cardiac accelerator nerves to the sinoatrial node (SAN), atrioventricular node
and most of the cardiac muscle, while parasympathetic fibres reach the heart in
the vagus nerve. Action potentials in the sympathetic nerve fibres result in a
release of noradrenaline, which binds to Β1-adrenoreceptors on the cardiac
muscle fibres. They respond by activating an excitatory G protein, causing
increased cAMP, which triggers the opening of Na+ and Ca2+ channels. This
speeds the rate of depolarisation of the cardiac muscle cells, as they can reach
threshold potential more quickly, and therefore the contraction of the heart
muscle cells occurs at an increased rate, resulting in increased blood pressure.
Conversely heart rate is slowed, and so blood pressure decreased, by
parasympathetic stimulation. Parasympathetic nerve fibres release
acetylcholine, which binds to muscarinic cholinergic receptors that activate a G
protein in the SAN cells, that has the opposite effect of the G protein stimulated
by the sympathetic nervous system. Its α subunit inhibits adenylate cyclase, and
therefore reduces cellular cAMP levels and the βγ subunit opens potassium
channels in the cell membrane, hyperpolarising the cell and making the time
taken to reach threshold potential longer, so the heart rate decreases, and blood
pressure decreases as a result. Parasympathetic stimulation of the heart muscle
has little effect on the force of contraction of the heart, whereas noradrenaline
released by sympathetic nerve fibres acts on contractile muscle fibres in the
ventricles to increase the force of contraction of the heart, causing an increased
stroke volume and therefore blood pressure. The sympathetic system has
another way of increasing blood pressure that does not involve nerve fibres
releasing neurotransmitters directly to the heart; using the hormone adrenaline.
Some preganglionic sympathetic fibres synapse onto chromaffin cells in the
adrenal medulla, which are triggered by acetylcholine secreted by the fibres to
release adrenaline into the blood. Adrenaline, like noradrenaline, works on G
protein coupled adrenergic receptors, and brings about a very similar response
to noradrenaline in the heart muscle cells. Blood pressure= cardiac output x
vascular resistance. I have described how cardiac output can be controlled by the
PNS and SNS, vascular resistance can also be altered//. LINKY LINKY
EFFECT ON BLOOD VESSELS
The sympathetic system is largely responsible for control of blood pressure via
vasomotion; changes in blood vessel diameter, while the parasympathetic
system has a less significant role in this way of controlling blood pressure.
Changing the diameter of blood vessels changes blood pressure since it affects
vascular resistance. Vascular resistance is determined by friction of the blood
with the walls of the blood vessels, the length of the vessels, and the viscosity of
the blood, as well as most significantly the radius of the blood vessels; where the
resistance decreases as the radius increases. This is expressed in, Poiseuille’s
Law; Resistance=(length of vessel x viscosity of blood)/(internal radius of
vessel)4 where length and viscosity are virtually constant, a small change in
radius will cause vascular resistance to change significantly. Blood vessel radius
can be altered by vasoconstriction and dilation. Sympathetic stimulation can
have opposite effects on blood vessel radius dependent on the hormone or
neurotransmitter that is acting. Noradrenergic sympathetic nerves to the blood
vessels maintain a base level of vasoconstriction, the sympathetic tone (tonic
contraction exerted on vessels by smooth muscle), which maintains total
peripheral resistance and therefore arterial blood pressure. The tone can be
increased through release of more noradrenaline, which acts on α1 receptors, to
cause vasoconstriction – a decrease in the radius of the vessels, which results in
an increase in peripheral vascular resistance and hence an increase in the
arterial blood pressure. Withdrawal of the sympathetic tone increases vessel
radius, promoting vasodilation. In contrast to noradrenaline, adrenaline,
secreted from the adrenal glands in response to sympathetic stimulation,
constricts some blood vessels and dilates others, dependent on the type of
adrenergic receptors present and the concentration of the hormone. Adrenaline
generally results in vasoconstriction of peripheral circulations, helping to
maintain arterial blood pressure, with the exception of triggering vasodilation of
blood vessels in skeletal muscle, and causing vasodilation when at a high
concentration. While sympathetic stimulation is the main way in which arterial
blood pressure is controlled through vasomotion, the PNS has quite a minimal
effect on the blood pressure through action on blood vessels. Parasympathetic
nerves only affect blood vessels in certain regions, such as the salivary glands,
which only represent a subset blood circulation. They cause vasodilation of
arteries via an indirect method involving local factors. When acetylcholine is
released by the parasympathetic nerve fibres, it stimulates the endothelium of
the arteries to produce and release nitric oxide, which diffuses to smooth
muscles to cause vasodilation, resulting in a decrease in blood pressure.
CONCLUSION-
In conclusion, the SNS and PNS control blood pressure through altering cardiac
output and vascular resistance. The SNS increases cardiac output through both
hormonal and nervous stimulation to increase heart rate and stroke volume,
while the PNS decreases cardiac output by causing a decreased heart rate. The
SNS has a greater role than the PNS in maintainance and control of blood
pressure through vasomotion; which alters vascular resistance. The ways in
which the PNS and SNS control blood pressure are highly contrasting, generally
having opposing affects and acting by different mechanisms. This antagonistic
pair of systems is required in order to maintain the blood pressure within
certain range, where in general the PNS stimulates if blood pressure too high,
sympathetic stimulated if blood pressure too low.