Renin–angiotensin system

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.[2][3]

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 the circulation. Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to angiotensin I, which has no biological function on its own.[4] Angiotensin I is subsequently converted to the active angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs.[5] Angiotensin II has a short life of about 1 to 2 minutes. Then, it is rapidly degraded into angiotensin III by angiotensinases which are present in red blood cells and vascular beds in many tissues.

Angiotensin III increases blood pressure and stimulates aldosterone secretion from the adrenal cortex; it has 100% adrenocortical stimulating activity and 40% vasopressor activity of angiotensin II. Angiotensin IV also has adrenocortical and vasopressor activities.

Angiotensin II is a potent vasoconstrictive peptide that causes blood vessels to narrow, resulting in increased blood pressure.[6] Angiotensin II also stimulates the secretion of the hormone aldosterone[6] 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.

If the RAS is abnormally active, blood pressure will be too high. There are several types of drugs which include ACE inhibitors, angiotensin II receptor blockers (ARBs), and renin inhibitors that interrupt different steps in this system to improve blood pressure. These drugs are one of the primary ways to control high blood pressure, heart failure, kidney failure, and harmful effects of diabetes.[7][8]

  1. ^ Boron WF, Boulpaep EL, eds. (2003). "Integration of Salt and Water Balance (pp. 866–867); The Adrenal Gland (p. 1059)". Medical Physiology: A Cellular And Molecular Approach. Elsevier/Saunders. ISBN 978-1-4160-2328-9. OCLC 1127823558. Archived from the original on 9 April 2022. Retrieved 8 April 2022.
  2. ^ Lappin S, Fountain JH (5 May 2019). "Physiology, Renin-Angiotensin System". NCBI. NIH. PMID 29261862. Archived from the original on 29 April 2019. Retrieved 9 May 2019.
  3. ^ Nakagawa P, Gomez J, Grobe JL, Sigmund CD (January 2020). "The Renin-Angiotensin System in the Central Nervous System and Its Role in Blood Pressure Regulation". Current Hypertension Reports. 22 (1): 7. doi:10.1007/s11906-019-1011-2. PMC 7101821. PMID 31925571.
  4. ^ Kumar A, Fausto A (2010). "11". Pathologic Basis of Disease (8th ed.). Saunders Elsevier. p. 493. ISBN 978-1-4160-3121-5. OCLC 758251143. Archived from the original on 9 April 2022. Retrieved 8 April 2022.
  5. ^ Golan D, Tashjian A, Armstrong E, Armstrong A (15 December 2011). Principles of Pharmacology – The Pathophysiologic Basis of Drug Therapy. Lippincott Williams & Wolters. p. 335. ISBN 978-1-60831-270-2. OCLC 1058067942. Archived from the original on 9 April 2022. Retrieved 8 April 2022.
  6. ^ a b Yee AH, Burns JD, Wijdicks EF (April 2010). "Cerebral salt wasting: pathophysiology, diagnosis, and treatment". Neurosurg Clin N Am. 21 (2): 339–352. doi:10.1016/j.nec.2009.10.011. PMID 20380974.
  7. ^ Bakris GL (November 2022). "High Blood Pressure: Heart and Blood Vessel Disorders". Merck Manual Home Edition. Archived from the original on 5 November 2010. Retrieved 6 June 2008.
  8. ^ Solomon SD, Anavekar N (2005). "A Brief Overview of Inhibition of the Renin–Angiotensin System: Emphasis on Blockade of the Angiotensin II Type-1 Receptor". Medscape Cardiology. 9 (2). Archived from the original on 15 December 2019. Retrieved 6 June 2008.
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