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Discipline | Medical Sciences |
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Language | English |
Edited by | Graham MacGregor |
Publication details | |
History | 2000–present |
Publisher | |
Frequency | Quarterly |
yes | |
2.271 (2013) | |
Standard abbreviations | |
ISO 4 | J. Renin-Angiotensin-Aldosterone Syst. |
NLM | J Renin Angiotensin Aldosterone Syst |
Indexing | |
CODEN | JRAAAG |
ISSN | 1470-3203 (print) 1752-8976 (web) |
LCCN | 2001243059 |
OCLC no. | 61677440 |
Links | |
Journal of the Renin-Angiotensin-Aldosterone System is a peer-reviewed academic journal that publishes papers in the field of Peripheral Vascular Disease. The journal's editors are Graham MacGregor and Peter Sever. It has been in publication since 2000 and is currently published by SAGE Publications.
Journal of the Renin-Angiotensin-Aldosterone System is a resource for biomedical professionals, including basic scientists and clinicians, primarily with an active interest in the renin-angiotensin-aldosterone system in humans and other mammals. The journal publishes original research and reviews on the normal and abnormal functions of the system. Journal of the Renin-Angiotensin-Aldosterone System also publishes research on other peptides, such as vasopressin, the natriuretic peptides and the kallikrein-kinin system.
Journal of the Renin-Angiotensin-Aldosterone System is abstracted and indexed in, among other databases: SCOPUS, and the Social Sciences Citation Index. According to the Journal Citation Reports , its 2013 impact factor is 2.271. [1]
Angiotensin-converting-enzyme inhibitors are a class of medication used primarily for the treatment of high blood pressure and heart failure. This class of medicine works by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.
Renin, also known as an angiotensinogenase, is an aspartic protease protein and enzyme secreted by the kidneys that participates in the body's renin-angiotensin-aldosterone system (RAAS)—also known as the renin-angiotensin-aldosterone axis—that increases the volume of extracellular fluid and causes arterial vasoconstriction. Thus, it increases the body's mean arterial blood pressure.
The renin-angiotensin system (RAS), or renin-angiotensin-aldosterone system (RAAS), is a hormone system that regulates blood pressure, fluid, and electrolyte balance, and systemic vascular resistance.
Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure. It is part of the renin–angiotensin system, which regulates blood pressure. Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys.
Atrial natriuretic peptide (ANP) or atrial natriuretic factor (ANF) is a natriuretic peptide hormone secreted from the cardiac atria that in humans is encoded by the NPPA gene. Natriuretic peptides are a family of hormone/paracrine factors that are structurally related. The main function of ANP is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized and secreted by cardiac muscle cells in the walls of the atria in the heart. These cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume.
Angiotensin-converting enzyme, or ACE, is a central component of the renin–angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II. Therefore, ACE indirectly increases blood pressure by causing blood vessels to constrict. ACE inhibitors are widely used as pharmaceutical drugs for treatment of cardiovascular diseases.
The angiotensin II receptors, (ATR1) and (ATR2), are a class of G protein-coupled receptors with angiotensin II as their ligands. They are important in the renin–angiotensin system: they are responsible for the signal transduction of the vasoconstricting stimulus of the main effector hormone, angiotensin II.
Essential hypertension is a form of hypertension without an identifiable physiologic cause. It is the most common type affecting 85% of those with high blood pressure. The remaining 15% is accounted for by various causes of secondary hypertension. Essential hypertension tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Hypertension can increase the risk of cerebral, cardiac, and renal events.
The baroreflex or baroreceptor reflex is one of the body's homeostatic mechanisms that helps to maintain blood pressure at nearly constant levels. The baroreflex provides a rapid negative feedback loop in which an elevated blood pressure causes the heart rate to decrease. Decreased blood pressure decreases baroreflex activation and causes heart rate to increase and to restore blood pressure levels. Their function is to sense pressure changes by responding to change in the tension of the arterial wall. The baroreflex can begin to act in less than the duration of a cardiac cycle and thus baroreflex adjustments are key factors in dealing with postural hypotension, the tendency for blood pressure to decrease on standing due to gravity.
Endothelins are peptides with receptors and effects in many body organs. Endothelin constricts blood vessels and raises blood pressure. The endothelins are normally kept in balance by other mechanisms, but when overexpressed, they contribute to high blood pressure (hypertension), heart disease, and potentially other diseases.
11-Deoxycorticosterone (DOC), or simply deoxycorticosterone, also known as 21-hydroxyprogesterone, as well as desoxycortone (INN), deoxycortone, and cortexone, is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as a precursor to aldosterone. It is an active (Na+-retaining) mineralocorticoid. As its names indicate, 11-deoxycorticosterone can be understood as the 21-hydroxy-variant of progesterone or as the 11-deoxy-variant of corticosterone.
Angiotensin II receptor type 1(AT1) is a Gq/11-coupled G protein-coupled receptor (GPCR) and the best characterized angiotensin receptor. It is encoded in humans by the AGTR1 gene. AT1 has vasopressor effects and regulates aldosterone secretion. It is an important effector controlling blood pressure and volume in the cardiovascular system. Angiotensin II receptor blockers are drugs indicated for hypertension, diabetic nephropathy and congestive heart failure.
Renin inhibitors are pharmaceutical drugs inhibiting the activity of renin that is responsible for hydrolyzing angiotensinogen to angiotensin I, which in turn reduces the formation of angiotensin II that facilitates blood pressure.
Pathophysiology is a study which explains the function of the body as it relates to diseases and conditions. The pathophysiology of hypertension is an area which attempts to explain mechanistically the causes of hypertension, which is a chronic disease characterized by elevation of blood pressure. Hypertension can be classified by cause as either essential or secondary. About 90–95% of hypertension is essential hypertension. Some authorities define essential hypertension as that which has no known explanation, while others define its cause as being due to overconsumption of sodium and underconsumption of potassium. Secondary hypertension indicates that the hypertension is a result of a specific underlying condition with a well-known mechanism, such as chronic kidney disease, narrowing of the aorta or kidney arteries, or endocrine disorders such as excess aldosterone, cortisol, or catecholamines. Persistent hypertension is a major risk factor for hypertensive heart disease, coronary artery disease, stroke, aortic aneurysm, peripheral artery disease, and chronic kidney disease.
Phlebology, The Journal of Venous Disease, is a peer-reviewed medical journal covering research on vascular disease. It is published by SAGE Publications and is an official journal of the American College of Phlebology, the Australasian College of Phlebology, the Venous Forum of the Royal Society of Medicine, the European Venous Forum, and the Benelux Society. The editor-in-chief is Alun Davies.
Angiology is a peer-reviewed academic journal that publishes papers in the field of Vascular disease. The journal's editor is Dimitri P. Mikhailidis. It has been in publication since 1950 and is currently published by SAGE Publications.
Diabetes and Vascular Disease Research is a peer-reviewed academic journal that publishes papers in the field of Peripheral vascular disease. The journal's editor is Peter Grant. It has been in publication since 2004 and is currently published by SAGE Publications.
Perfusion is a peer-reviewed academic journal that publishes papers in the field of cardiology. The journal's editor is Prakash P. Punjabi. It has been in publication since 1986 and is currently published by SAGE Publications.
EMA401 is a drug under development for the treatment of peripheral neuropathic pain. Trials were discontinued in 2015, with new trials scheduled to begin March, 2018. It was initially established as a potential drug option for patients suffering pain caused by postherpetic neuralgia. It may also be useful for treating various types of chronic neuropathic pain EMA401 has shown efficacy in preclinical models of shingles, diabetes, osteoarthritis, HIV and chemotherapy. EMA401 is a competitive antagonist of angiotensin II type 2 receptor (AT2R) being developed by the Australian biotechnology company Spinifex Pharmaceuticals. EMA401 target angiotensin II type 2 receptors, which may have importance for painful sensitisation.
L-163,491 is an experimental drug which acts as a partial agonist of angiotensin II receptor type 1, and with lower affinity as an agonist of angiotensin II receptor type 2, mimicking the action of angiotensin II. Its practical applications to date have been limited to scientific research into the function of the angiotensin receptor system, but it has been suggested as a potential therapeutic agent for the treatment of inflammation of the lungs associated with certain viral diseases such as COVID-19.
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