Does Hypertension Have a Genetic Basis Research Paper

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Introduction

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, no repinephrine is existent and stress is felt especially acutely.

Phenotype and Genotype

It is unknown what 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.

Pathophysiological Processes

The pathophysiological processes of hypertension are very complex. The kidney plays an integral role and is also the target organ of the processes while other organs also play a part in the processes. Genetics, neurohormonal systems (sympathetic nervous system, rennin-angiotensin-aldosterone system), along with obesity, and salt intake from diet are all factors in the onset (Hamrahian, 2017).

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Hypertension progresses from essential to established stages and typically begins as prehypertension in persons aged 10 to 30 years old and advances 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 a-adrenoceptor stimulation and/or increased peptides (angiotension or endothelins). Cytosolic calcium can build up to cause vascoconstriction and can lead to ventricular diastolic dysfunction. It is also hypothesizd that “resetting of pressure natriuresis plays a key role in causing hypertension” and is characterized by parallel shift to high blood pressure along with salt-intensive blood pressure increase (Foex, Phil, Sear, 2004).

Genetic Predispositions

Both hypertension and type 2 diabetes commonly co-exist in a patient and there is some genetic predisposition in these patients for developing cardiovascular disease (Qibin, Forman, Jensen et al., 2012). Geller (2004) shows that both genetics and environment may predispose an individual to hypertension. The genetic factors are not well understood, however (the environmental factors are: salt intake and exercise, for example).

The molecular basis of monogenic disorders that impact blood pressure have received more attention in recent years and a variety of genomic polymorphisms have been linked genetically to hypertensive phenotypes—though the linkage is still unclear to researchers in regards to how the relationship unfolds. However, as Geller (2004) reports, “genome-wide linkage studies have also been performed, and these have linked regions on chromosome 12p and 17q to hypertension in large cohort studies; these loci are intriguing because they have previously been linked to monogenic blood pressure disorders as well. Nevertheless, no precise genetic polymorphism affecting blood pressure has been identified….....

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