Journal of Cholesterol and Heart Disease

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Short Communication - Journal of Cholesterol and Heart Disease (2022) Volume 6, Issue 6

Hypertension: a detailed study.

Alexander Jonah*

Department of Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, UK

*Corresponding Author:
Alexander Jonah
Department of Cardiovascular and Metabolic Health,
University of Glasgow,
Glasgow, UK
E-mail:[email protected]

Received:19-Nov-2022, Manuscript No. AACHD-22-84351; Editor assigned: 21-Nov-2022, PreQC No. AACHD-2284351(PQ); Reviewed:05-Dec-2022, QC No. AACHD-22-84351; Revised:09-Dec-2022, Manuscript No. AACHD-22-84351(R); Published:16-Dec-2022, DOI: 10.35841/aachd-6.6.129

Citation: Jonah A. Hypertension: A detailed study. J Cholest Heart Dis 2022;6(6):129

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Abstract

The most significant modifiable risk factor for global all-cause morbidity and death is systemic arterial hypertension, which is also linked to an elevated risk of Cardiovascular Disease (CVD). Though proper treatment of hypertension lowers the overall burden of disease and death, less than half of persons with hypertension are aware of their condition, and many more that are aware but are not treated or are treated insufficiently. The intricate interaction of environmental and pathophysiological variables, which have an impact on several systems, as well as genetic predisposition, is the aetiology of hypertension. Accurate standard Blood Pressure (BP) measurement, evaluation of patients' predicted risk of atherosclerotic cardiovascular disease, detection of target organ damage, identification of secondary causes of hypertension, and the presence of comorbidities, such as CVD and kidney disease, are all parts of evaluating patients with hypertension.

Keywords

Blood pressure, Hypertension, Vascular disorder.

Introduction

The leading single cause of death and disability from all causes worldwide is hypertension, which is the most frequent preventable risk factor for cardiovascular disease; including coronary heart disease, heart failure, stroke, myocardial infarction, atrial fibrillation, and peripheral artery disease, Chronic Kidney Disease (CKD) and cognitive impairment. Starting as low as 115/75mmHg, far within the range that is regarded as normotensive, there is a graded and on-going link between blood pressure and an increased risk of cardiovascular disease. Reduced disease load and increased lifespan among the global population are both largely dependent on effective hypertension prevention and treatment. It is crucial to take into account a person's projected atherosclerotic CVD risk while treating hypertension rather to only their blood pressure level since those with high CVD risk acquire [1].

Lowering blood pressure and avoiding hypertension and its CVD consequences can be accomplished by lifestyle changes, such as dietary adjustments and increased physical activity. Angiotensin-Converting Enzyme (ACE) inhibitors, angiotensin II receptor blockers, dihydropyridine calcium channel blockers, and thiazide diuretics are the first line antihypertensive medications. Pharmacological therapy is very effective in lowering blood pressure and preventing CVD outcomes in the majority of patients [2].

Aldosterone is a key player in the development of hypertension because it activates the amiloride-sensitive sodium channel, also known as the Epithelial Sodium Channel (ENaC), and stimulates renal Na+ reabsorption in the cortical collecting duct by binding to the mineralocorticoid receptor without directly altering gene expression. Other non-epithelial effects of aldosterone include vasoconstriction, hypertension, and endothelial dysfunction. These include vascular remodelling, fibrosis, vascular extracellular matrix deposition, vascular smooth muscle cell proliferation, and elevated oxidative stress [3].

Lack of natriuretic peptides encourages hypertension. The pro-ANP and pro-BNP ANP and BNP precursors are transformed into their active forms by the serine protease corin, which is mostly expressed in the heart. Corin deficiency has been linked to salt-sensitive hypertension, cardiac failure, and volume overload. Additionally, type 2 diabetes mellitus and insulin resistance are made more likely by a lack of natriuretic peptide. It is thought that the overexpression of the natriuretic peptide scavenger receptor NPR-C in adipose tissue contributes to the association between obesity and natriuretic peptide insufficiency. The metabolic syndrome is a collection of conditions that includes high blood pressure, high fasting blood sugar, abdominal obesity, high triglycerides, and microalbuminuria and increases the risk of CVD and diabetes mellitus. Natriuretic peptides have therapeutic potential for the metabolic syndrome [4].

A major factor in the development of hypertension and the resulting damage to target organs is inflammation. Increased vascular permeability and the production of powerful mediators such reactive oxygen species, NO, cytokines, and metalloproteinases are related with inflammation. Cytokines play a role in the formation of neo-intima, a new or thickened layer of arterial intima, which reduces the diameter of resistance vessels lumens (small arteries and arterioles, which are the main blood vessels involved in controlling blood pressure) and encourages vascular fibrosis, increasing vascular resistance and stiffness. By enhancing local angiotensinogen and angiotensin II production, as well as by encouraging salt and volume retention in hypertension, cytokines can have an impact on renal tubular function. The breakdown of the extracellular matrix is accelerated by matrix metalloproteinases [5].

Conclusion

Reducing the burden of diseases linked to high blood pressure can be accomplished in large part by increasing the effectiveness of pharmacological therapy. The greatest impact could be attained by delivering and distributing affordable, efficient single-pill combinations of 2 or 3 drugs to low-income and middle-income countries where the burden of hypertension is considerable and where any such therapies are currently either largely unavailable or unaffordable. This is in contrast to focusing on rare secondary causes of hypertension or the best management of treatment-resistant hypertension.

References

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  3. Ehret GB, Ferreira T, Chasman DI, et al. The genetics of blood pressure regulation and its target organs from association studies in 342,415 individuals. Nat Genet. 2016;48(10):1171-84.
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