The Physiology of Blood Pressure Control

The Physiology of Blood Pressure Control

The Physiology of Blood Pressure Control 150 150 Peter

The Physiology of Blood Pressure Control

Discussion Prompt

Initial Post: Describe the physiology of blood pressure control. Causes of Primary Hypertension may include overactivity of the SNS; overactivity of the RAAS; alterations in other neurohumoral mediators of blood volume and vasomotor tone such as ANP, BNP, and adrenomedullin; inflammation; a complex interaction involving insulin resistance and endothelial function; and obesity-related hormonal changes

Select 3 of the above potential causes and explain the pathophysiologic mechanisms of primary hypertension.

Identify the organ damage that can occur as a result of Hypertension. Describe the pathophysiologic process of the organ damage.

Orthostatic hypotension can occur as an adverse effect of medications used to manage hypertension. Describe the pathophysiologic process that causes orthostatic hypotension.

Sample Paper

Describe the physiology of blood pressure control

Blood pressure is a measurement of the pressure in the circulatory system throughout the heart’s pumping cycle. A wide range of factors might alter the body’s needs. It is impossible to predict how a person’s blood pressure will fluctuate throughout the day (Shahoud, et al,. 2019). The process of homeostasis maintains blood pressure. Automated blood pressure monitors, stethoscopes, and sphygmomanometers are used to measure blood pressure. mmHg (millimetres of mercury) is the unit of measurement and is expressed as a pair of numbers (e.g., 120/80). There are short-term and long-term approaches to managing high blood pressure levels.

Short-term blood pressure regulation is under the direction of the ANS. Baroreceptors sense variations in blood pressure. The carotid sinus arch and the aorta’s wall are both home to these baroreceptors. When the blood artery wall is strained by high arterial pressure, baroreceptors are activated. These baroreceptors transmit data to the autonomic nervous system, which in turn processes it. The efferent parasympathetic fibers of the ANS then lower the heart rate (vagus nerve). As a result, blood pressure is reduced. Baroreceptors detect a drop in artery pressure, which prompts a sympathetic reaction (Shahoud,et al,. 2019). Blood pressure rises as a result of an increase in heart rate and cardiac contractility. In the long run, baroreceptors are unable to control blood pressure. It’s because when blood pressure returns to a safe level, the system that activates the baroreceptors resets itself.

In contrast, the renin-angiotensin-aldosterone (RAAS) system aids in the long-term control of the blood pressure level. This hormone is produced in the kidney by the granule cells of the juxtaglomerular apparatus. Angiotensinogen is converted to angiotensin I by the enzyme renin, which acts as a catalyst. After this, angiotensin II is produced by the angiotensin-converting enzyme (ACE).

One of the most effective vasoconstrictors is angiotensin II. Due to its effects on the kidney, it enhances salt uptake by this particular part of the system. Re-absorption of sodium by the sodium-hydrogen exchanger is accomplished. Aldosterone production is aided by angiotensin II as well. Aldosterone increases the expression of epithelial sodium channels in the distal convoluted tubule, which aids in salt and water retention. Sodium-potassium ATPase activity is also increased by aldosterone. As a result, the electrochemical gradient for sodium-ion transport has increased. As more salt accumulates in renal tissue, osmosis transports it to the bloodstream. This leads to increased blood volume and blood pressure due to reduced water excretion. Bradykinin, a potent vasodilator, is likewise broken down by ACE. As a result, the constricting impact is amplified by the breakdown of bradykinin. This further strengthens the rise in blood pressure overall.

Select 3 of the above potential causes and explain the pathophysiologic mechanisms of primary hypertension.

High blood pressure without a known underlying cause is called essential hypertension or primary hypertension (Saxena & Saxena, 2018). Obesity-related hormonal alterations, an overactive SNS, and an overactive RAAS are the fundamental causes. Obesity decreases parasympathetic tone and increases sympathetic activity. A higher heart rate, less variability in the heart rate, and less baroreflex sensitivity are linked to these autonomic activity changes, which in turn cause hypertension .In addition, research shows that increased SNS activity contributes to primary hypertension caused by obesity. Obese and hypertensive people have enhanced SNS activity in specific but not all tissues. Additionally, the RAAS may also have a role in developing essential hypertension. Oxidative brain stress activates the RAAS, increasing sympathetic outflow. Aldosterone and angiotensin II operate in the brain to start this force, increasing sympathetic flow and blood pressure.

Identify the organ damage that can occur as a result of hypertension. Describe the pathophysiologic processes of organ damage.

When primary hypertension persists for an extended period, it can lead to complex hypertension, which has harmful consequences for many organs. The heart, kidneys, brain, and eyes are only a few of the vital organs that might be harmed by severe hypertension (Monticone, et al,. 2018). Additionally, the body’s extremities are affected. This develops as a result of blood vessel wall damage throughout the body. There is hyperplasia and hypertrophy of the smooth muscle cells in the arteries, arterioles, and arterioles. Furthermore, tunica intima and media fibrosis occur due to a process known as vascular remodeling. Endothelial dysfunction, Angiotensin II, catecholamines, insulin resistance, and long-term hypertension inflammation all contribute to vascular remodeling. Fibrosis causes organs to get less blood flow. Organs are severely affected by the absence of blood flow.

Heart failure left ventricular hypertrophy and Myocardial ischemia can occur when the heart’s myocardium is overworked and undernourished due to diminished blood circulation through the coronary arteries (Monticone, et al,. 2018). Lack of blood flow elevated arteriolar pressure, RAAS and SNS activation can harm the kidneys. Renal failure and end-stage renal disease can result from this. Reduced blood flow to the brain reduces the oxygen supply required for optimal brain function. Swelling and hardening of the blood vessels in the eye can lead to vision loss. Retinal hemorrhages and hypertensive retinopathy are possible side effects. Having weak aortic artery walls might cause a dissection.

Orthostatic hypotension can occur as an adverse effect of medications used to manage Hypertension. Describe the pathophysiologic process that causes orthostatic hypotension.

Blood normally pools in the veins of the legs and trunk due to the gravitational tension of suddenly standing (Magkas et al,. 2019). BP is reduced as a result of a short-term reduction in venous return. Quick recovery to standard blood pressure (BP) is achieved by activating autonomic reflexes in the aortic arch and carotid sinus. The consciousness of the sympathetic nervous system causes an increase in heart rate and contractility and a rise in blood vessel tone. The heart rate rises when parasympathetic (vagal) inhibition is likewise inhibited. If you are standing for an extended period, you may notice a drop in your blood pressure and heart rate, although these changes are usually short-lived. While standing, the renin-angiotensin-aldosterone system and vasopressin (an antidiuretic hormone) release promote salt and water retention and raise blood volume.



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