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(USMLE topics) Renal control of blood pressure via RAAS. This video is available for instant download licensing here: 🤍 Voice by: Ashley Fleming ©Alila Medical Media. All rights reserved. Support us on Patreon and get early access to videos and free image downloads: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. The renin–angiotensin–aldosterone system, RAAS, is a hormonal system that controls blood pressure. While baroreflex is a short-term response to sudden changes in blood pressure, RAAS is responsible for long-term regulation. In the kidneys, within the walls of afferent arterioles, there are specialized cells producing prorenin called juxtaglomerular cells. Upon activation by a drop in blood pressure, prorenin is cleaved to form renin, which is released into the blood. Renin converts a plasma protein called angiotensinogen, produced by the liver, into angiotensin I, a peptide of 10 amino acids. Angiotensin I is further converted into angiotensin II, an 8-amino acid peptide, by the angiotensin-converting enzyme, ACE, predominantly present in the lungs and kidneys. Angiotensin II is a hormone. It binds to angiotensin II receptors in tissues to exert various effects: - It promotes sodium reabsorption in proximal convoluted tubules of the kidneys. - It stimulates vasoconstriction in systemic arterioles. - It induces the release of aldosterone from the adrenal cortex. Aldosterone promotes sodium and water retention in the kidneys. - In the central nervous system, angiotensin II has several effects: + It acts on the hypothalamus to stimulate thirst and encourage water intake. + It induces the posterior pituitary to release antidiuretic hormone, which promotes water retention by the kidneys. + It reduces the sensitivity of the baroreceptor response to increased blood pressure, so that this response would not counteract the effect of RAAS. All these actions lead to an increase in blood volume and blood pressure. Angiotensin II is short-lived with a half-life of 1 to 2 minutes. It is degraded into angiotensin III and IV, which have lesser effects. Overactive or inappropriately activated RAAS is a cause for hypertension. RAAS is a frequent target of anti-hypertensive drugs. ACE inhibitors and angiotensin receptor blockers are common treatment for hypertension.
This animation focuses on the renin angiotensin aldosterone system (RAAS), a classic endocrine system that helps to regulate long-term blood pressure and extracellular volume in the body. Many aspects of cardiovascular disease progression can be directly linked to the RAAS system. Mechanisms such as vascular inflammation, generation of reactive oxygen species and alterations of endothelial function are all known to play a role in atherosclerosis.
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One of the proteins present in the blood is called angiotensinogen. This is a short protein produced by the liver and is inactive; it just circulates in the blood. However, when renin acts on angiotensinogen it converts it into another shorter protein called angiotensin I. As angiotensin I passes through the lungs it is converted into angiotensin II by an enzyme called angiotensin converting enzyme (ACE). Angiotensin II is a powerful vascular vasoconstrictor; this will increase peripheral resistance which will in turn increase blood pressure. In addition to increasing BP by direct vasoconstriction angiotensin II also stimulates the secretion of aldosterone from the adrenal cortex. This will increasethe amount of sodium reabsorbed from the renal tubules and so increase levels of sodium in the blood. As mentioned, increased levels of sodium increases the osmotic potential of the blood and so it attracts more water. This means more water is retained in the plasma increasing blood volumes. These increased volumes will increase venous return and so blood pressure. Conversely, lower amounts of angiotensin II will reduce aldosterone secretion leading to more sodium excretion. This will lower sodium levels in the blood leading to lowered blood volumes and so lower BP. If the systemic blood pressure is increased the pressure in the afferent arteriole will also be increased. This will be detected by the JGA cells which will respond by reducing renin secretion. When less renin is present in the blood, more angeotensionogen will remain in inactive form. This renin-angiotensin-aldosterone mechanism allows the kidneys to regulate their own blood flow to an extent. When an organ regulates itself in this way it is called autoregulation. If for any reason the kidneys over-secrete renin blood pressure will be raised. An abnormally high BP is termed hypertension. Renin excess probably explains most cases of chronic hypertension. You may have come across ACE inhibiting drugs; these inhibit ACE (angiotensin converting enzyme) and so inhibit the conversion of angiotensin I into angiotensin II. If there is less angiotensin II there will be less vasoconstriction and less secretion of aldosterone and so blood pressure will be lowered.
GET LECTURE HANDOUTS and other DOWNLOADABLE CONTENT FROM THIS VIDEO SUPPORT US ON PATREON OR JOIN HERE ON YOUTUBE. 🤍 When the plasma sodium concentration is lower than normal or the renal blood flow is reduced, the juxtaglomerular cells in the kidneys convert prorenin (an intracellular protein) into renin, which is then secreted directly into the circulation. Plasma renin then cuts a short, 10 amino acid long, peptide off a plasma protein known as angiotensinogen. The short peptide is known as angiotensin I.[2] Angiotensin I is then converted, by the removal of 2 amino acids, to form an octapeptide known as angiotensin II, by the enzyme angiotensin-converting enzyme (ACE) found in the lung capillaries. Angiotensin II is a potent vaso-active peptide that causes arterioles to constrict, resulting in increased arterial blood pressure.[3] Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex.[3] Aldosterone causes the tubular epithelial cells of the kidneys to increase the reabsorption of sodium ions from the tubular fluid back into the blood, while at the same time causing them to excrete potassium ions into the tubular fluid which will become urine. RELATED TOPICS renin catalysis protein chemical compound organic compound endocrine system polymer blood pressure angiotensin enzyme Renin-angiotensin system, physiological system that regulates blood pressure Renin is an enzyme secreted into the blood from specialized cells that encircle the arterioles at the entrance to the glomeruli of the kidneys (the renal capillary networks that are the filtration units of the kidney). The renin-secreting cells, which compose the juxtaglomerular apparatus, are sensitive to changes in blood flow and blood pressure. The primary stimulus for increased renin secretion is decreased blood flow to the kidneys, which may be caused by loss of sodium and water (as a result of diarrhea, persistent vomiting, or excessive perspiration) or by narrowing of a renal artery. Renin catalyzes the conversion of a plasma protein called angiotensinogen into a decapeptide (consisting of 10 amino acids) called angiotensin I. An enzyme in the serum called angiotensin-converting enzyme (ACE) then converts angiotensin I into an octapeptide (consisting of eight amino acids) called angiotensin II. Angiotensin II acts via receptors in the adrenal glands to stimulate the secretion of aldosterone, which stimulates salt and water reabsorption by the kidneys, and the constriction of small arteries (arterioles), which causes an increase in blood pressure. Angiotensin II further constricts blood vessels through its inhibitory actions on the reuptake into nerve terminals of the hormone norepinephrine. Watch Again 🤍 SUBSCRIBE 🤍 -~-~~-~~~-~~-~- CHECK OUT NEWEST VIDEO: "Nucleic acids - DNA and RNA structure " 🤍 -~-~~-~~~-~~-~-
In this video, Dr Mike explains the renin Angiotensin Aldosterone System in under 2 minutes!
🤍 - This tutorial explores the Renin-Angiotensin-Aldosterone System, its role in Blood Pressure, the enzymes, involved, and how drugs act upon the system. For more entirely FREE medical tutorials visit 🤍
🤍 Describes at a basic level the roles Angiotensin II plays in the body. And also how it is formed. What organs it interacts with 🤍
Renin-angiotensin-aldosterone system (RAAS) nursing review for how this system manages the blood pressure via the kidneys. The RAAS helps manage the blood pressure, especially when the blood pressure is too low. When the body senses the blood pressure is too low the sympathetic nervous system will sends nerve impulses to the juxtaglomerular cells in the kidneys. These cells will release renin. When renin enters the circulation, it will cause a substance in the liver to become activated called angiotensinogen. Angiotensinogen will turn into angiotensin I. As angiotensin I presents in the system it will signal to ACE (angiotensin-converting-enzyme) to convert the angiotensin I into angiotensin II. Angiotensin II is a major vasoconstrictor that will cause vasoconstriction and trigger the adrenal gland and pituitary gland to release substances to help increase blood volume. The adrenal gland will release aldosterone, which will cause the kidneys to keep sodium and water. The pituitary gland will release ADH (antidiuretic hormone), which will cause the kidneys to keep water. All of this together will increase systemic vascular resistance and blood pressure. #RAAS #reninangiotensinaldosteronesystem #RAASnursing Quiz: 🤍 Notes: 🤍 More Review Lectures: 🤍 Nursing Gear: 🤍 Instagram: 🤍 Facebook: 🤍 Twitter: 🤍 Website: 🤍 Popular Playlists: NCLEX Reviews: 🤍 Fluid & Electrolytes: 🤍 Nursing Skills: 🤍
✨In this video, I talk about Renin, Angiotensin II, Aldosterone, the Antidiuretic Hormone and how the whole system works together. I hope it helps!☀️ 🌟What's in this video? 0:00 - Intro 0:14 - The Juxtaglomerular Apparatus (JGA) 0:56 - The Renin Angiotensin Pathway 1:50 - Actions of Angiotensin II 3:16 - Indirect Effects of Angiotensin on Aldosterone 4:02 - Indirect Effects of Angiotensin on ADH 4:24 - Factors stimulating the RAAS 6:32 - RAAS in low blood volume 7:10 - RAAS in high salt intake ✨ Other videos you may need : 🔅Starling Forces in the Glomerulus: 🤍 🔅 Summary of Hormones acting on the kidney: 🤍 🔅 Proximal Convoluted Tubule: 🤍 🔅 Distal Convoluted Tubule and Collecting Duct: 🤍 💫 For more videos like this, subscribe to my channel! Byte Size Med: 🤍 📚Factual References & for Further Reading: - Guyton and Hall Textbook of Medical Physiology - Ganong’s Review of Medical Physiology - Costanzo’s Textbook of Physiology - First Aid for the USMLE, 2020 edition - Openstax Anatomy and Physiology 🤍 - Openstax Biology 🤍 (The last two are links to open-source references. They are NOT affiliate links) 🌤 Note: These are just a collection of my notes. So use them the way you would use borrowed notes from a friend. 📝 The images in this video are hand-drawn for illustration and explanation only.✍️ Hence, they may not be anatomically accurate. I am just one person making these videos. If there are any errors, that is unintentional. I try super hard to avoid them. Please let me know if you find any, so it gets clarified for other viewers. Science constantly evolves and changes. New discoveries are made everyday. So some of the information in these videos may become outdated. If you notice that, please let me know so I can update them. ⚡️Disclaimer: These videos are NOT a substitute for a medical textbook. Textbooks are written by experts (which I do not claim to be), edited, proofread and referenced. Please use them. The information has been sourced from multiple references as mentioned above. I draw all the pictures myself. But if I have inadvertently infringed on any copyright, that is completely unintentional. I only make these videos to impart education. If I have accidentally violated copyright in any way, do let me know so I can make the necessary changes or give credit to anyone who is owed the same. These videos are NOT intended for patient education. They are NOT a substitute for diagnosis and treatment by a licensed medical professional. Always seek the advice of a qualified health care provider for any questions you may have regarding any medical condition, so that they can address your individual needs. 🔅They are ONLY meant to help students of medicine and health sciences with studying, and should be used for just that purpose and absolutely nothing else. Byte Size Med. All Rights Reserved.
Learn the three major triggers for Renin production by the Juxtaglomerular cells. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai. Watch the next lesson: 🤍 Missed the previous lesson? 🤍 NCLEX-RN on Khan Academy: A collection of questions from content covered on the NCLEX-RN. These questions are available under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 United States License (available at 🤍 About Khan Academy: Khan Academy offers practice exercises, instructional videos, and a personalized learning dashboard that empower learners to study at their own pace in and outside of the classroom. We tackle math, science, computer programming, history, art history, economics, and more. Our math missions guide learners from kindergarten to calculus using state-of-the-art, adaptive technology that identifies strengths and learning gaps. We've also partnered with institutions like NASA, The Museum of Modern Art, The California Academy of Sciences, and MIT to offer specialized content. For free. For everyone. Forever. #YouCanLearnAnything Subscribe to Khan Academy’s NCLEX-RN channel: 🤍 Subscribe to Khan Academy: 🤍
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MINT Merch: 🤍 (Thank you for the support) Hey Guys! You are watching an educational video about the Renin Angiotensin Aldosterone System. Don't forget to share this video with your classmates so that more people can see this awesome video. Medical-Surgical Nursing Book: 🤍 Share our YouTube Channel: 🤍 Share this video: 🤍 Follow us on Instagram: 🤍 Share this video: 🤍 Disclaimer: The information in this video is a general compilation of different nursing books. This video is not intended to replace information you have obtained from school or your facility. Refer to your facility's policies and procedures for specific guidelines. Equipment used: 1. Camera: 🤍 2. Microphone: 🤍 3. Camera Cage: 🤍 4. Monitor: 🤍
This test measures the level of renin in the blood. Renin is a hormone made by the kidneys. It controls the production of another hormone called aldosterone, which is made in the adrenal glands. Aldosterone helps manage blood pressure and maintain healthy levels of potassium and sodium in the body. If renin and aldosterone levels are not normal, it can be a sign of a serious adrenal gland disorder. Because the two hormones work together, an aldosterone test is often done along with a renin test. What is it used for? A renin test is used to find out if the adrenal glands are making too much or too little aldosterone. The test is especially useful in diagnosing primary aldosteronism (PA), also known as primary hyperaldosteronism or Conn syndrome, causes high blood pressure. If not treated, high blood pressure increases the risk of stroke, heart attack, and kidney failure. Why do I need a renin test? You may need a renin test if you've been diagnosed with high blood pressure, Its especially needed high bp doesn't respond well to standard blood pressure medicines. The test can show whether PA is causing the condition. Sometimes PA causes low potassium levels, so you may also need this test if you have symptoms of low potassium. These include: Cramps Weakness Excessive thirst Fatigue Headache What do the results mean? higher than normal amount of renin, may mean you have: Addison disease, a condition in which your adrenal glands don't make enough of certain hormones Cirrhosis, scarring of the liver Dehydration lower than normal amount of renin, may mean you have: Primary aldosteronism (PA) Kidney disease
AMBOSS, Wissen – von Medizinern für Mediziner. 🤍 Flüssigkeitsvolumen, Osmolarität und Blutdruck hängen direkt miteinander zusammen und werden gemeinsam in engen Grenzen reguliert. Dabei ist das Zusammenspiel der Enzymen und Hormonen wichtig, die die Menge an resorbiertem Natrium und Wasser in der Niere auf die Verhältnisse im Körper abstimmt. Die Rede ist vom sogenannten RAAS. In dieser Folge des Auditors erfährst du wie genau die Enzyme und Hormone zusammenarbeiten und welche Wirkungen sie haben. Und mehr zum Thema gibt es wie immer im entsprechenden AMBOSS-Kapitel: 🤍 Inhalt: 00:00 – Einleitung 00:57 – Zusammenspiel 02:29 – Wirkungen 04:25 – ADH 05:24 – ANP AMBOSS ist das ideale Nachschlagewerk für Ärztinnen und Ärzte im klinischen Alltag und das perfekte Lernsystem für Medizinstudierende. AMBOSS enthält das Wissen aller Fachgebiete - so ausgearbeitet und vernetzt, dass Mediziner unmittelbar leitliniengerechte Antworten auf ihre Fragestellung erhalten. #ambossmed #auditor #RAAS #Niere
Angiotensin-Converting Enzyme 2 (ACE2) is an important component of the Renin-Angiotensin System which controls blood pressure but is now gaining recognition in the fields of virology and epidemiology for the role it plays in SARS-CoV-2 infection. By understanding the function of ACE2, we can better understand the role it may play in the seemingly unconnected symptoms of COVID-19. This video is part of the Research Integrated Science Education (RISE) Program that is funded by SENS Research Foundation and Dalio Philanthropies. The program is designed to introduce high school students to aging research and laboratory concepts, such as experimental design and data interpretation, within core curriculum standards. To learn more about RISE and to access additional functionalities such as the transcript glossary function, visit 🤍
شرح مفصل خطوة بخطوة لسستم Renin Angiotensin Aldosterone لاتنسونا من صالح دعائكم
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What is the Renin Angiotensin Aldosterone System (RAAS) and how to remember it easily. For more fun information, visit 🤍 or 🤍tootRN.com
🤍 has diagrams, notes, and a link to Quizlet flashcards: 🤍 The kidneys sense low blood pressure and low blood volume and release an enzyme called Renin. Renin converts angiotensinogen (a plasma protein made by the liver) into angiotensin I. Angiotensin Converting Enzyme (ACE) converts angiotensin I into angiotensin II. Angiotensin II has three main effects: 1. constricts arterioles to raise blood pressure. 2. stimulates the adrenal cortex to release aldosterone. Aldosterone then causes the kidneys to reabsorb more salt. This causes water to be retained and increases blood volume and thus blood pressure. 3. stimulates the posterior pituitary gland to release antidiuretic hormone, also known as vasopressin. Vasopressin causes the kidneys to retain more water, which raises blood volume and therefore raises blood pressure. Drug Targets to Lower Blood Pressure in RAAS: 1. ACE inhibitors block ACE action 2. ARA (angiotensin receptor antagonists) block Angiotensin II from binding its targets 3. Aldo Antagonists 4. Vaptans inhibit vasopressin 5. Renin inhibitors
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A review of the normal physiology of sodium, potassium, and water. Major topics covered include the renin angiotensin aldosterone system, the hypothalamic pituitary adrenal axis, ADH (antidiuretic hormone), and the natriuretic peptides.
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Hello Friends Welcome to Rj Medical Education In this video I explained about :- #reninangiotensinaldosteronesystem #renin #angiotensin #aldosterone system in #hindi #renin function #aldosterone #angiotensin work #how aldosterone work #reinin functions in #bloodpressure #aldosterone #functions in blood pressure #role of #angiotensin in #bloodpressure If you have any queries regarding this video, Please drop your comment in comment box, I would love to answer. If you like the video, Please like, share and subscribe channel. Thank you. #rjmedicaleducation #coachingfreeindia #rajneetmedicaleducation
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Presented By: Dr. Brandy Gunsolus Speaker Biography: Dr. Brandy Gunsolus received her BS degree in Chemistry from Southeastern Louisiana University, a BS degree in Clinical Laboratory Science from LSU Health Sciences Center – New Orleans, an MS degree and Doctor of Clinical Laboratory Science degree from Rutgers University. She is currently over Pathology Utilization, is the Physician/Laboratory Liaison, oversees the Immunology and Toxicology Laboratories, and is Director of Specimen Referral at Augusta University Medical Center. She also serves on the Doctoral Review Committee for National Accreditation Agency for Clinical Laboratory Science and is the American Society for Clinical Laboratory Science National delegate to the Coalition to Improve Diagnosis in Medicine. She is Chair for the American Society for Clinical Laboratory Science National Scientific Assembly for Laboratory Administration/Industry/Consulting/Accreditation/Quality Assurance, Vice-Chair for the American Society for Clinical Laboratory Science National Patient Safety committee and President of the South Carolina chapter for American Society for Clinical Laboratory Science. Webinar: Updates on Primary Aldosteronism Screening and Use of Direct Renin Webinar Abstract: Primary aldosteronism (PA) is the most common form of secondary hypertension, caused by hyperactivity in one or both of the adrenal glands that leads to inappropriate aldosterone production. The prevalence of PA among general and resistant hypertensive populations ranges from 5-20%. PA is considered highly treatable and potentially curable. As such, the Endocrine Society guidelines recommend screening for PA in high risk populations using the plasma aldosterone/plasma renin ratio (ARR). It is generally accepted that both the plasma renin and aldosterone levels tend to fall with advancing age and plasma renin decreases more than aldosterone; consequently, the ARR increases in the elderly which supports the need for age-specific ARR cutoffs. Traditionally, renin has been measured by a plasma renin activity (PRA) radioimmunoassay or liquid chromatography tandem mass spectrometry (LC-MS/MS). Direct renin concentration (DRC) immunoassays, also known as plasma renin concentration (PRC), have recently become more popular because of numerous benefits including walk-away automation, shorter turnaround times, and excellent reproducibility compared to PRA. In this webinar, we will review the key differences between PRA and DRC assays and discuss the utility of proposed age-specific ARR cutoffs for PA screening calculated using direct renin measurement. Earn PACE Credits: 1. Make sure you're a registered member of LabRoots (🤍 2. Watch the webinar on the LabRoots Website (🤍 3. Click Here to get your PACE credits (Expiration date – SEP 23, 2023): (🤍 LabRoots on Social: Facebook: 🤍 Twitter: 🤍 LinkedIn: 🤍 Instagram: 🤍 Pinterest: 🤍 SnapChat: labroots_inc
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🤍 Describes how, when, where Renin is secreted from. And how Pro-renin coverts to renin.
When the #bloodpressure drops suddenly, the #kidney senses that fall in pressure and activates the #RAAS, How? Let's have a look. Learn more: 🤍 _ Key moments- 0:00 Start 0:38 what is RAAS? 1:20 How RAAS works? 1:53 Renin 2:25 Angiotensin 3:15 RAAS on Kidney 3:45 RAAS on adrenal cortex 4:35 RAAS on arterioles 4:55 RAAS on Heart 5:26 RAAS on Brain 6:25 Function of RAAS 6:47 RAAS mechanism in kidney 7:20 Next antihypertensives Within the afferent arterioles of the kidney, specialized cells called juxtaglomerular or JG cells contain prorenin. Prorenin, which is a protein that constitutes a precursor for renin, the hormone that activates the renin–angiotensin system, which serves to raise 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. As the name suggests, the renin–angiotensin–aldosterone system is compromised of these 3 hormones, renin, angiotensin, and aldosterone. RAAS is frequently manipulated to treat various heart conditions like hypertension, heart failure, diabetes mellitus, and acute myocardial infarction. In the next videos, we will learn about the antihypertensive class of drugs, including, ACE inhibitors, ARBs, and renin inhibitors. Thank you for watching. Please subscribe and support us to learn more.
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As two Biology/Health Majors destined to a future in the medical practices, my college buddy and I wrote a song to remember the Renin-Angiotensin-Aldosterone Pathway. This music video was an afterthought used to showcase the song. Enjoy. Copyright 2007 (c) Matt Kaske-Cirigliano & Eric Klotz LYRICS: Chorus: Renin Angiotensin Renin Aldosterone Renin Angiotensin Renin Aldosterone Pathway Verse 1: Dehydrate No sodium And hemorrhage (Oh st!) Decreases blood volume Decreasing blood pressure Juxtaglomerular cells Of the kidneys... Renin Verse 2: Angiotensinogen Increases angiotensin (through ACE!) Vasoconstricting arterioles Pressure Verse 3: Adrenal cortex Increases aldosterone The kidneys do the rest Increasing blood volume pressure
Thanks for watching.... I hope it helped you to understand it... Do not forget to like, share among your friends and please subscribe... The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance. When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into circulation. Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to angiotensin I.[3] Angiotensin I is subsequently converted to angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs.[4] Angiotensin II is a potent vasoconstrictive peptide that causes blood vessels to narrow, resulting in increased blood pressure.[5] Angiotensin II also stimulates the secretion of the hormone aldosterone[5] from the adrenal cortex. Aldosterone causes the renal tubules to increase the reabsorption of sodium which in consequence causes the reabsorption of water into the blood, while at the same time causing the excretion of potassium (to maintain electrolyte balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure.
In meinen Videos möchte ich heilpraktikerspezifisches Basiswissen vermitteln, welches notwendig ist um die Prüfung zu bestehen. Das Renin-Angiotensin-Aldosteron-System, kurz RAAS, reguliert den Flüssigkeits- und Elektrolythaushalt des Körpers und wirkt somit in entscheidender Weise auf den Blutdruck ein. Vorsicht!! Ich erhebe nicht den Anspruch auf Vollständigkeit in meinen Videos.
#Plasma_Renin_Therapy #hypertension #enzyme_inhibitor #angiotensin_receptor_blocker #calcium_channel_blockers #thiazide_type_diuretic #Primary_Hypertension Plasma Renin-guided Therapy benefits Patients of Primary Hypertension Hyper tension is a common public health problem worldwide affecting approximately 25.3% of Indian population. The Eighth Joint National Committee guidelines recommend initiating treatment of hypertension with one of the four agents that is angiotensin-converting enzyme inhibitor (ACEI), angiotensin receptor blocker (ARB), calcium channel blockers, or thiazide-type diuretic, with a target BP of less than 140/90 mm Hg. But there is something new to discuss today. Get the latest medical and health news at medicaldialogues.in Follow us on Twitter: 🤍 Facebook: 🤍 Instagram: 🤍 LinkedIn: 🤍 Website: 🤍
🤍 Describes how Angiotensinogen converts to Angiotensin I then II. And looks at what gets cleaved off the structure of these polypeptide chains. It also talks about chymase and how it functions as an converting enzyme.
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