Essay On Blood Pressure Notes

How is blood pressure physiologically regulated? How can this be modulated by drugs?

Blood pressure

The mean arterial pressure is calculated by cardiac output x peripheral resistance. Changes in either of these factors lead to changes in blood pressure. In an average person the blood pressure measured by a sphygomomanometer is 120/80, however these measurements often vary during the day and increases with age due to atherosclerosis. During excercise and intense emotion the release of systemic hormones causes an increase in blood pressure whereas during sleep there is a drop in blood pressure. However deviations in blood pressure from its set point leads to autoregulatory mechanisms which restore it to its normal level. It is important for the body to maintain a high constant blood pressure within a narrow range as it ensures optimum organ perfusion and efficient glomerular filtration. It also overcomes high tissue pressure in eye. If the pressure is too low the patient is in shock whereas the pressure is too high the patient is hypertensive and if pressure is at either of these two extremes local blood flow can no longer be regulated by myogenic and metabolic autoregulation. Short term regulation of blood pressure, which takes seconds to minutes occurs through neural pathways and targets the heart, vessels and the adrenal medulla. In comparison long term regulation targets mostly the kidneys which control the extracellular fluid. In patients whose biological mechanisms that regulate blood pressure have failed require drugs are required to maintain a constant blood pressure.

One way blood pressure is regulated is through neural reflexes. During rest the C1 neurons of the medulla vasomotor centre exerts a tonic activity on the sympathetic vasoconstrictor nerves which results in basal vasoconstriction. The activity of C1 neurons was shown when clonidine was injected which bound to imidazole receptors and resulted in an inhibition of the C1 neurons and this led to a decrease in blood pressure. When there is an acute change in blood pressure there is a change in the activity of baroreceptors which results in a neural reflex that brings mean arterial pressure back to normal. Baroreceptors are stretch receptors that detect expansion in vascular walls. The activity of baroreceptor reflexes was shown by an expirement carried out by Heyman. When adrenaline was injected into dogs there was a subsequent rise in blood pressure but due to the neural reflex this was followed by a decrease in heart rate. To show that is was neuronal activity rather than hormones in the blood stream that resulted in bradycardia Heyman cross perfused 2 dogs where one dog had nerves connected but its blood supply to its head coming from the 2^nd dog. When the 1^st dog was injected with adrenaline there was a decrease in heart rate showing that it was neuronal activity.

Baroreceptor control of arterial pressure

High pressure baroreceptors are found at the carotid sinus and the aortic arch. The carotid sinus is very elastic and is located on the internal carotid artery just above the position where the carotid artery bifurcates into the internal and external artery. The second high pressure baroreceptor is found in the aortic arch which is also elastic but has a high compliance that allows it to distend during left ventricular ejection. Both of the aortic arch and carotid sinus baroreceptors are made up of a mixture of A and C fibres. A fibres have a large diameter, are fast conducting, myelinated and have a low threshold. These fibres are active at normal blood pressure. Whereas C fibres which are more abundant, are myelinated, slow conducting, have a small diameter and high thresholds. Having a mixture of the two types of muscle fibres allows recruitment of different fibres according to the blood pressure. The terminals of these fibres express nonselective cation channels which are from the TRP family.

When there is an increase in transmural pressure difference the blood vessel is enlarged and this deforms TRPC1 channels which results in a depolarising inward current and forms the receptor potential. To show that these channels are stretch sensitive rather than pressure sensitive, the vessels was prevented from being stretched which resulted in the failure to open the TRPC1 channels even when there is an increase in transmural pressure.

The receptor potential is a graded response where the amplitude of the depolarisation is proportional to the amount the blood vessel is stretched. The depolarisation produced results in a biphasic response as there is an initial large increase in depolarisation, known as the dynamic component, followed by steady depolarisation. If the carotid sinus or the aortic arch is distended rapidly it results in a high frequency of action potentials which is then followed by a lower frequency of action potentials. In the carotid sinus the impulses travel through the sinus nerve which joins the glossopharngeal nerve. Likewise the aortic arch baroreceptor transmits its impulses through the depressor branch of the vagus nerve. In both cases the afferent nerves transmit impulses to the medullary cardiovascular centre and synapse with neurons in the nucleus tractus solitarii by releasing glutamate which binds to AMPA receptors. This results in the stimulation of inhibitory interneurons which originate in the nucleus tractus solitarii and synapse with C1 neurons in the vasomotor area. The inhibition of the C1 neurones results in a decrease in the amount of neurotransmitter released that results in vasoconstriction. This results in a decrease in basal activity of the sympathetic vasoconstriction which causes vasodilation and causes a reduction in a total peripheral resistance. The afferent nerve fibres in the nucleus tractus solitarii also innervate excitatory interneurons which synapse with the cardioinhibitory area which includes the nucleus ambiguous and dorsal motor nucleus of the vagus. Innervation...

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