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How Aldosterone and Renin Levels Cause Hypertension in African Americans

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The paper should focus on how aldosterone and renin levels cause hypertension in African Americans All sources need to be no more than 10 years old. At least 7 primary sources. The rest can be review. Even if you can complete 5 pages at least by Wednesday March 16th that will be ok but I’d need a I know by noon eastern time

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Hypertension in the African American Community
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Hypertension in the African American Community
Hypertension is the foremost foundation of CVD mortality in the United States of America. CVD affects about 29% of adults corresponding to over 75 million people. Hypertension, also known as high blood pressure, is in an insistent and progressive increase. According to Ukpabi and Ewelike (2017), the SBP and DBP connote diagnostic criteria for hyperon. On the other hand, they may differ contingent on the nonappearance of existing infections. The financial liability of hypertension in the USA is colossal, often developing questions concerning its significant influence on health inequality. In addition, it is linked to infections such as CVD and terminal renal infection.
Furthermore, African Americans individuals and other ethnic groups of African origins record increased blood pressure starting in childhood and a higher incidence and prevalence of high blood pressure across their lives. According to Mozaffarian et al. (2015), the age-adjusted incidence of African-American individuals is 45%, expressively more sophisticated than in other customs. For example, Non-Hispanic white people represent 32% and 30% Hispanics. According to Williams (2014), Primary conjecturers of hypertension exist in African American people. For instance, weakened elasticity is more widespread in African Americans than white people. In their study, African American people have more likely to possess a suppressed renin phenotype and an increased SBP.
On the other hand, Tu et al. (2018) mention in their study that aldosterone sensitivity increased with age among African American individuals. Moreover, the sensitivity of the aldosterone is linked with plasma (blood) concentration and the renin quotient, signifying a possible increase in mineralocorticoid receptor activity with age. With close relation to the analysis above, the paper discusses how the levels of aldosterone and renin cause hypertension in African American people. 
The Prevalence of High Blood Pressure (Hypertension)
African Americans start developing hypertension earlier than their white counterparts. They are also highly likely to develop intractable hypertension and increased degrees of precipitate hypertensive health impediments such as heart infection, stroke, and CKD (Merai et al., 2016). Notably, African American individuals endure three-fold increased mortality rates due to high blood pressure and cardiovascular infections, leading to most deaths recorded in care facilities. NHANES (2022) mentions that though African Americans show improved blood pressure control, the general control of BP remains below average nationally. Between 1994 and 2004, blood pressure was adequately managed in about 35% white people and about 29% African American descent. 
Factors Underwriting to the Pathogenesis of High Blood Pressure in African Americans
Understanding the diagnosis of hypertension, poor blood pressure control and augmented intensity of medical treatment, and resilient hypertension are crucial factors distinguishing hypertension among AAs “African Americans” from whites. Similarly, hypertensive analytic inertia is explained as a letdown to examine the fundamental basis of hypertension, a continuing problem in African American individuals with a heart infection (James et al., 2014). Furthermore, adrenocortical hyperplasia was established as a common factor in African Americans and other patients of African origin. It suggests a possibility of aldosterone as a crucial factor underwriting the pathogenesis of elevated blood pressure in African American people. There is little understanding concerning the genetic multiplicity of high blood pressure in African American people, especially psychosocial blood volume. Despite that, numerous researchers have emphasized genes involved in changed renal sodium management in the volume loading and kidneys, which are critical players in advancing reduced renin high blood pressure.  
Renin and Aldosterone
Diversity may occur within the African ancestry population. The medical and genetic information of African-Americans and other African origins ought to be analyzed, construed, and contrasted with a lot of attentiveness. James et al. (2014) analyzed the blood pressure of about 1,500 government employees and established an increased incidence of hypertension among black and brown people. The black and brown people represented 49.3% and 38.2%. Importantly, Chor et al. (2015) established that high blood pressure (hypertension) features in Brazilian brown individuals are similar to the African Americans. African American individuals excrete or expel sodium load gradually and less competently than white people leading to the dominance of the “renin-aldosterone-angiotensin” system, also known as RAAS, because of capacity or volume loading that generally starts to retain sodium amount. A frequent cause of high blood pressure is low-renin hypertension, and it has an incidence rate of 20 to 30%—the incidence rate increases in African American individuals. According to Tu et al. (2014), African Americans always recorded reduced “plasma renin action and aldosterone in normotensive in age groups with blood pressure relating with plasma aldosterone.” 
How Aldosterone and Renin Levels Cause Hypertension in African Americans
Black hypertensive individuals incline to preserve water and salt. The kidney is vital in maintaining water balance and sodium. Typically, kidneys filter about 25,000 mmol of Natrium (Sodium) daily. It also excretes about 1% of the filtered load. On the other hand, the everyday ingestion of Sodium arrays from 20 to 40 mmol in standard hunter-gatherer settings and about 3000 mmol daily in modern communities. The Barter and Gitelman syndrome mentioned any imperfection or faultiness in sodium reabsorption. The kidney cannot sufficiently reabsorb Natrium (Sodium) in the dense rising loop of Henle, and distal convoluted tubules can lead to a fatal outcome for the infected individual (patient) (Rao et al. 2020). For example, it can trigger the “renin-angiotensin-aldosterone” system and chronic hypokalemia. Sodium and hypertension are scarce for individuals residing in a normal hunter-gatherer society.
Such individuals have a crucial sodium balance. A minor defect in sodium reabsorption can prevent circulatory homeostasis, leading to environmental pressure in identifying genes that can actively preserve sodium. The matters can be considered a crucial factor that helped Blacks survive and travel from Africa to America in slave ships (Tu et al., 2018). The Liddle syndrome demonstrates widespread hereditary infections, where the over-performing of the renal tubular ENaC “epithelial sodium channel” arises from triggering alterations in the B- and Y-chains. It leads to hypertension since sodium retention, potassium excretion, and reduced aldosterone and renin levels. As the water follows Natrium (Na+), the mechanism is liable for more excellent water retention. 
Aldosterone Levels
Plasma aldosterone is linked with blood pressure, insulin resistance, and waist circumference. It raises the probab...
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