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).
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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