This paper examines hypertension as a chronic elevation of blood pressure with potentially fatal consequences. It surveys the complex genotype-phenotype relationships involved in essential hypertension, including the roles of the autonomic nervous system, the kidney, and neurohormonal systems. The paper discusses the angiotensinogen (AGT) gene as the most studied genetic factor linked to hypertension, reviews patterns of inheritance, and explores genetic mutations tied to the renin-angiotensin system. Racial and ethnic predispositions, particularly among African Americans, are addressed alongside a broad range of risk factors. The paper concludes with an interdisciplinary management plan emphasizing lifestyle modification and patient education.
Hypertension is the chronic elevation of blood pressure that can lead to organ failure and even mortality. Cardiac output creates blood pressure, but in patients with hypertension, cardiac output is increased. The autonomic nervous system helps to regulate blood pressure, but in patients with hypertension, norepinephrine levels are altered and stress is felt especially acutely.
It is unknown which genes cause hypertension. Moreover, as Korner (2010) points out, "their identification is unlikely to be realized with current genetic approaches, because of ambiguities in the genotype-phenotype relationships in these polygenic disorders" (p. 841). Korner (2010) also notes that in the case of hypertension, the phenotype is "not just an aggregate of traits, but needs to be related to specific components of the circulatory control system at different stages" of hypertension (p. 841).
Korner (2010) does show that some studies are underway to better understand the genotype-phenotype relationship for hypertension. These studies focus on "major differences in circulatory control in the two main syndromes of EH: (1) stress-and-salt-related EH (SSR-EH) — a constrictor hypertension with low blood volume; (2) hypertensive obesity — SSR-EH plus obesity" (p. 841). Korner (2010) states that each of these differences "is initiated through sensitization of central synapses linking the cerebral cortex to the hypothalamic defense area" and that "several mechanisms are probably involved, including cerebellar effects on baroreflexes" (p. 841). More study needs to be conducted in order to better understand the mechanism, however.
The pathophysiological processes of hypertension are very complex. The kidney plays an integral role and is also a target organ of these processes, while other organs also contribute. Genetics, neurohormonal systems (the sympathetic nervous system and the renin-angiotensin-aldosterone system), along with obesity and dietary salt intake are all factors in the onset of hypertension (Hamrahian, 2017).
Hypertension progresses from essential to established stages and typically begins as prehypertension in persons aged 10 to 30 years old, advancing to early hypertension in persons aged 20 to 40 years old. Established hypertension typically occurs in people aged 30 to 50 years old.
Hypertension causes vascular tone to be heightened as a result of alpha-adrenoceptor stimulation and/or increased peptides (angiotensin or endothelins). Cytosolic calcium can accumulate to cause vasoconstriction and can lead to ventricular diastolic dysfunction. It is also hypothesized that "resetting of pressure natriuresis plays a key role in causing hypertension" and is characterized by a parallel shift to higher blood pressure along with a salt-sensitive blood pressure increase (Foex, Phil, & Sear, 2004).
"Genomic linkages, inheritance patterns, and unknowns"
"AGT gene function and evolutionary mutation context"
"Epidemiology, racial disparities, and recent research focus"
"Risk factors, interdisciplinary plan, and best-practice recommendations"
You’re 30% through this paper. Sign up to read the remaining 4 sections.
Sign Up Now — Instant Access Already a member? Log inAlways verify citation format against your institution’s current style guide requirements.