Journal of Cholesterol and Heart Disease

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Editorial - Journal of Cholesterol and Heart Disease (2021) Volume 5, Issue 1

Hypertension A dangerous risk factor for cardiovascular diseases.

Armani Marvin*

Department of Clinical Pharmacy and Therapeutic, Applied Science Private University, Amman 11931-166, Jordan

Corresponding Author:
Dr. Armani Marvin
Department of Clinical Pharmacy and Therapeutic,
Applied Science Private University,
Amman 11931-166, Jordan
E. mail: [email protected]

Accepted date: 16 November, 2021

Citation: Marvin A. Hypertension A dangerous risk factor for cardiovascular diseases. J Cholest Heart Dis. 2021;5(1):4.

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About the Study

Hypertension is the most common adjustable threat factor for cardiovascular complaint and death, and lowering blood pressure with antihypertensive medicines reduces target organ damage and prevents cardiovascular complaint issues. Despite a plethora of available treatment options, a substantial portion of the hypertensive population has unbridled blood pressure. The unmet need of controlling blood pressure in this population may be addressed, in part, by developing new medicines and bias/ procedures to treat hypertension and its comorbidities. Interventional treatments that are witnessing preclinical or clinical testing for hypertension treatment. New medicine classes, e.g., impediments of vaso peptidases, aldosterone synthase and answerable epoxide hydrolase, agonists of natriuretic peptide A and vasoactive intestinal peptide receptor 2, and a new mineralocorticoid receptor antagonist are in phase II/ III of development, while impediments of amino peptidase A, dopamine β-hydroxylase, and the intestinal Na/ H exchanger 3, agonists of factors of the angiotensin- converting enzyme2/ angiotensin (1-7)/ Mamas receptor axis and vaccines directed toward angiotensin II and its type 1 receptor are in phase I or preclinical development. The two main interventional approaches, transcatheter renal denervation and baro reflex activation remedy, are used in clinical practice for severe treatment resistant hypertension in some countries. Renal denervation is also being estimated for treatment of colorful comorbidities, e.g., habitual heart failure, cardiac arrhythmias and habitual renal failure. New interventional approaches in early development include carotid body ablation and arteriovenous fistula placement. Importantly, none of these new medicine or device treatments has been shown to help cardiovascular complaint issues or death in hypertensive cases.

Anti-Aldosterone Agents

Aldosterone is a mineralocorticoid that regulates electrolyte and volume homeostasis in normal subjects and, when elevated, can contribute to the development of hypertension and a variety of affiliated pathologies, including myocardial hypertrophy and fibrosis and HF.10 The star effector of aldosterone action is the mineralocorticoid receptor (MR), a nuclear recap factor that's expressed at high situations in the cortical collecting conduit of the order. Actuated stimulate expression of sodium channels, performing in increased sodium and water reabsorption and potassium loss, leading ultimately to a volume expanded form of hypertension. Activation of MRs in redundant adrenal apkins, particularly the heart and blood vessels, also promotes the development of hypertension and CVD by up regulating NADPH oxidase and adding product of reactive oxygen species. This reduces the bioavailability of nitric oxide and leads to endothelial dysfunction .

Medium of action of anti-aldosterone agents . Aldosterone synthase impediments (ASIs), similar as LCI699, inhibit the rate limiting step of aldosterone product. Mineralocorticoid receptor agonists (MRAs), similar as finerenone, contend for the list spots of aldosterone and effectively drop blood pressure and aldosterone- intermediated gene recap. Both approaches have been shown to be useful in treating aldosteroneintermediated hypertension and vascular complaint. Aldosterone conflation, green; cortisol conflation, red; antialdosterone medicines, blue.

Aldosterone is synthesized from 11-deoxycorticosterone in the zona glomerulosa of the adrenal cortex via the action of a mitochondrial cytochrome P450 enzyme, aldosterone synthase, which is decoded by the CYP11B2 gene11. Aldosterone synthase catalyzes the final 3 rate- limiting way of aldosterone conflation (11β-hydroxylation of 11-deoxycorticosterone to form corticosterone, followed by 18-hydroxylation of corticosterone to form 18OH-corticosterone, and 18-oxidation of 18-OH corticosterone to form aldosterone). Cortisol conflation, which occurs in the zona fasciculata of the adrenal cortex, is intermediated by 11β-hydroxylase, which is decoded by the CYP11B1 gene CYP11B2 has a high sequence homology with CYP11B1, and both CYP11B2 and CYP11B1 partake an 11β-hydroxylase response, creating problems for those trying to design picky aldosterone synthase impediments.

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