Angiotensin II for the Treatment of Vasodilatory Shock

Ashish Khanna1, Shane W English1, Xueyuan S Wang1

  • 1From Anesthesiology Institute, Center for Critical Care and Department of Outcomes Research, Cleveland Clinic, Cleveland (A.K.); the Department of Medicine (Critical Care), University of Ottawa, and the Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa (S.W.E.); Division of Critical Care Medicine, Department of Anesthesiology, Duke University Medical Center, Durham, NC (X.S.W.); Regions Hospital, St. Paul, MN (K.H.); University of Tennessee College of Medicine, Chattanooga (J.T.); the Division of Nephrology, Baylor University Medical Center, Dallas (H.S.); the Department of Medicine, Emory University School of Medicine, Atlanta (L.W.B.); Inova Medical Center, Falls Church, VA (L.A.); the Department of Internal Medicine, University of California Davis School of Medicine, Sacramento (T.E.A.), the Division of Critical Care, Department of Anesthesiology, University of California Los Angeles, Los Angeles (D.W.B.), and La Jolla Pharmaceutical Company, San Diego (J.J., S.K., L.S.C., G.F.T.) - all in California; the Department of Pulmonary and Critical Care Medicine, Riverside Methodist Hospital, Columbus, OH (C.M.); the Division of Pulmonary and Critical Care Medicine, University of Maryland School of Medicine, Baltimore (M.T.M.); the Department of Surgery, Sunrise Hospital, Las Vegas (S.C.); Intensive Care Unit, Wellington Hospital, and Medical Research Institute of New Zealand, Wellington, New Zealand (P.J.Y.); the Division of Critical Care, Department of Medicine, Eastern Idaho Regional Medical Center, Idaho Falls (K.K.); the Department of Medicine, Pulmonary and Critical Care, Northwestern University Feinberg School of Medicine, Chicago (R.G.W.); the Department of Critical Care and Nephrology, King's College London, Guy's and St. Thomas' Hospital, London (M.O.); the Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh (R.M.); the Department of Medicine, Albert Einstein College of Medicine, and the Division of Critical Care Medicine, Montefiore Medical Center, Bronx, NY (M.N.G.); John Hunter Hospital, New Lambton Heights, and School of Medicine and Public Health, University of Newcastle, Callaghan, NSW (R.P.), the Department of Intensive Care, Wesley Hospital and Princess Alexandra Hospital, University of Queensland, St Lucia (B.V.), and School of Medicine, University of Melbourne, Parkville (R.B.), and the Intensive Care Unit, the Royal Melbourne Hospital, University of Melbourne (A.M.D.), Melbourne, VIC - all in Australia; the Division of Intensive Care Medicine, Department of Anesthesiology, Intensive Care, and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki (J.H.); INSERM UMR 995 LIRIC (Lille Inflammation Research Center), Centre Hospitalier Universitaire Lille, Critical Care Center and University of Lille School of Medicine, Lille, France (R.F.); and the Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Boston (B.T.T.).

Abstract

Related Concept Videos

Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
2.9K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.7K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
1.3K
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
2.4K
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.7K
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
511