Commentary Article - (2023) Volume 4, Issue 2
Received: 31-May-2023, Manuscript No. JAC-23-17071; Editor assigned: 02-Jun-2023, Pre QC No. JAC-23-17071 (PQ); Reviewed: 16-Jun-2023, QC No. JAC-23-17071; Revised: 21-Jun-2023, Manuscript No. JAC-23-17071 (R); Published: 28-Jun-2023, DOI: 10.35841/jac.4.2.18
Angiotensin is a part of the renin-angiotensin-aldosterone system (RAAS), a complex physiological pathway that helps maintain homeostasis. In addition to its role in blood pressure regulation, angiotensin has been implicated in various other physiological processes. This article explores the functions of angiotensin, its role in cardiovascular health, and its relevance to medical research and therapy.
Angiotensin, a peptide hormone, serves as a vital regulator of blood pressure and plays a broader role beyond cardiovascular function. The Renin-Angiotensin System (RAS) drives the production of angiotensin, which acts on blood vessels, kidneys, and various organs. Angiotensin II, the most potent form, constricts blood vessels, elevating blood pressure. It also stimulates the release of aldosterone, which increases sodium retention and potassium excretion, further impacting blood pressure regulation. Additionally, angiotensin exerts various non-cardiovascular effects, such as promoting inflammation, fibrosis, and oxidative stress. Dysregulation of the RAS and angiotensin has been implicated in hypertension, cardiovascular diseases, kidney dysfunction, and other pathologies.
The RAAS is a complex hormonal pathway involved in the regulation of blood pressure and fluid balance. It consists of several components, with angiotensin serving as a central player. The process begins when the enzyme renin, released by the kidneys, converts a protein called angiotensinogen, produced by the liver; into angiotensin I. Angiotensin I then converted to angiotensin II by the action of the angiotensin-converting enzyme primarily found in the lungs.
Angiotensin II is a potent vasoconstrictor, meaning it causes the narrowing of blood vessels. This constriction increases resistance to blood flow, leading to an increase in blood pressure. Angiotensin II also stimulates the release of the hormone aldosterone from the adrenal glands, which promotes sodium and water retention, further contributing to increased blood pressure. Through its actions on aldosterone, angiotensin II plays a crucial role in regulating fluid and electrolyte balance in the body. By promoting sodium reabsorption in the kidneys, it helps maintain proper fluid volume and electrolyte concentrations. Angiotensin II also affects the kidneys directly, where it constricts blood vessels within the kidney, leading to decreased blood flow and increased filtration of waste products. This helps maintain glomerular filtration rate and proper renal function. Angiotensin has been implicated in the development and progression of cardiovascular diseases, such as hypertension, heart failure, and atherosclerosis. Excessive activation of the RAAS system can lead to chronic elevation of blood pressure and contribute to the development of cardiovascular complications.
The involvement of angiotensin in blood pressure regulation and cardiovascular health has made it a target for therapeutic interventions. Several classes of medications have been developed to modulate the RAAS system and treat hypertension and other cardiovascular conditions. These include: These medications block the activity of ACE, preventing the conversion of angiotensin I to angiotensin II. By inhibiting angiotensin II production, ACE inhibitors help dilate blood vessels, lower blood pressure, and reduce the workload on the heart. These medications block the action of renin, the enzyme responsible for the initial conversion of angiotensinogen to angiotensin I. By inhibiting this step, direct renin inhibitors reduce the production of angiotensin II and lower blood pressure.
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The author’s declared that they have no conflict of interest.
Citation: Lu Z (2023) Angiotensin as a Key Regulator of Blood Pressure and Beyond. Autacoids J. 4:18.
Copyright: © 2023 Lu Z. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.