Chat with us, powered by LiveChat The physiology of blood pressure control results from several factors. Firstly, regulation comes from cardiac output pe | WriteDen

The physiology of blood pressure control results from several factors. Firstly, regulation comes from cardiac output pe

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The physiology of blood pressure control results from several factors. Firstly, “regulation comes from cardiac output per minute from the left ventricle along with systemic vascular resistance and stretching of blood vessel walls” (Parker & Atkins, 2018). These sensory receptors are known as the baroceptor reflex. According to Shahoud et al. (2021), baroceptors are a form of mechanoreceptor that become activated by the stretching of the vessel. This sensory information is conveyed to the central nervous system and used to influence peripheral vascular resistance and cardiac output. The autonomic nervous system regulates short term blood pressure while long term arterial pressure depends on the relationship between arterial pressure and the output of water and salt in one’s urine. Furthermore, the hormone aldosterone regulates salt and water in the body thereby having an effect on blood pressure. Next, antidiuretic hormone made in the hypothalamus, also known as vasopressin, constantly balances and regulates the water amount in the blood. “ADH mainly functions to increase free water reabsorption in the collecting duct of the nephrons in the kidney, causing an increase on plasma volume and arterial pressure” (Shahoud et al., 2021). Finally, the renin-angiotensin aldosterone system is essential in regulating and relies on several hormones to increase peripheral resistance and blood volume. This system begins with the release of renin from the juxtaglomerular cell in the kidney. According to Shahoud et al. (2021), they respond to decreased blood pressure, sympathetic nervous system activity, and reduced sodium levels within the distal convoluted tubes of the nephrons. Renin then enters the blood and combines with angiotensin and is converted into angiotensin I. Then, angiotensin I travels to the pulmonary vessels where it encounters the angiotensin-converting enzyme created in the endothelium and converts angiotensin I to angiotensin II. This angiotensin II uses vasoconstriction of arterioles throughout the body to increase arterial pressure.

One cause of primary hypertension is the overactivity of the renin-angiotensin-aldosterone system. This system is comprised of the related hormones, renin, angiotensin and aldosterone, that work in conjunction to regulate blood pressure and control inflammation. “These three act to elevate arterial pressure in response to decreased renal blood pressure, decreased salt delivery to the distal convoluted tubule, and/or beta-agonism” (Fountain & Lappin, 2021). However, overactivity of this system can lead to primary hypertension. According to Fountain and Lappin (2021), though the RAAS serves a critical function, it can be activated inappropriately in several conditions that may lead to the development of hypertension. One such condition is renal artery stenosis that results in a decreased amount of blood volume reaching one or both kidneys. “As a result, the juxtaglomerular cells will sense a decrease in blood volume, activating the RAAS. This can lead to an inappropriate elevation of circulating blood volume and arteriolar tone due to poor renal perfusion” (Fountain & Lappin, 2021). Another cause of primary hypertension is overactivity of the sympathetic nervous system.  According to Wyss and Carlson, the primary final common pathway for the nervous system’s contribution to hypertension is the sympathetic nervous system. The overactivity of this system can be the result of several factors occurring in the body. “Sympathetic nervous system overactivity may result from either inappropriately elevated sympathetic drive from brain centers, an increase in synaptically released neurotransmitters in the periphery, or amplification of the neurotransmitter signal at the target tissue” (Wyss & Carlson, 2001). Finally, inflammation can also lead to hypertension. Inflammation is the result of an injury or infection as a protective response from various cells. The inflammatory cascade response results in oxidative stress and endothelial dysfunction. Therefore, excessive inflammation can produce extremely harmful effects on the body leading to chronic diseases like hypertension. According to Savoia and Schiffrin. (2006), inflammatory processes are important participants in the pathophysiology of hypertension and cardiovascular diseases. In primary hypertension, blood flow is restricted due to increased peripheral vascular resistance. “Inflammatory markers, such as C-reactive protein, are associated with vascular lesions in humans, and are predictive of cardiovascular outcome” (Savoia & Schiffrin, 2006).

References

Fountain, J. H., & Lappin, S.L. (2021). Physiology, Renin angiotensin system. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK470410/

Parker, D. E., & Atkins, W. A. (2018). Blood pressure. Gale Encyclopedia of Nursing and Allied Health. (4th ed.), Gale. https://su.idm.oclc.org/login?url=https://search.credoreference.com/content/entry/galegnaah/blood_pressure/0?institutionId=6543

Savoia, C., & Schiffrin, E. (2006). Inflammation in hypertension. Current Opinion in Nephrology and Hypertension 15, 152-158. https://doi.org/10.1097/01.mnh.0000203189.57513.76

Shahoud, J. S., Sanvictores, T., & Aeddula, N. R. (2021). Arterial pressure regulation. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK538509/

Wyss, J. M., & Carlson, S. H. (2001). The role of the nervous system in hypertension. Curr Hypertens Rep 3(3), 255-262. https:// www.doi.org./10.1007/s11906_001-0048-0PMID:11353577

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  • Blood pressure supplies blood to all parts of the body as it is pumped through the heart. The systolic and desolate pressure helps to facilitate this movement resulting from the ventricular relaxation and contraction. However, the primary reason hypertension sometimes may characterize the functioning of the heart. Primary hypertension can be detrimental because it results from an overactive SNS, overactive RAAS, and hormonal changes among obese individuals. These occur when there is increased diastolic pressure.
    An individual with an overreactive SNS experienced a high possibility of developing paroxysmal sympathetic hyperreactivity. This is a condition associated with an increased risk of hypertension, especially because of our increasing activity with the sympathetic nervous system. This condition increases respiration rates and hatcheries that arise as primary symptoms of high blood pressure. The management of this condition requires incorporating diverse missions to increase the level of physical activities and healthy dietary practices (Sexana et al., 2018).
    An overactive renin-angiotensin-aldosterone system (RAAS) is also a major factor in high blood pressure. RAAS helps with the regulation of cardiovascular and renal functions. However, with primary high blood pressure, an increase in arterial pressure arises when the body fails to regulate extracellular fluid. When managing this condition, focused on incorporating both pharmacological and nonpharmacological measures focused on improving renal function.
    For obesity-related hormonal changes, they affect the body's general functioning because of the accumulation of fat in specific regions, which increases the risk of primary hypertension. This one of the changes is often defined by reducing parasympathetic tone and increased sympathetic activity. The negative effects are associated with numerous changes in outdoor genomic activity, contributing to a decline in heart rate variability. The best techniques of managing this condition will entail incorporating approaches aimed at reducing baroreflex sensitivity and individuals (Hall et al., 2015).
    References
    Hall, J. E., do Carmo, J. M., da Silva, A. A., Wang, Z., & Hall, M. E. (2015). Obesity-induced hypertension: interaction of neurohumoral and renal mechanisms. Circulation Research116(6), 991-1006.
    Saxena, T., Ali, A. O., & Saxena, M. (2018). Pathophysiology of essential hypertension: an update. Expert Review of Cardiovascular Therapy16(12), 879-887.
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