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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.