Cation Interdependency in Acute Stressor States
Abstract Acute stressor states are inextricably linked to neurohormonal activation which includes the adrenergic nervous system. Consequent elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K+ , Mg2+ and Ca2+ . Catecholamines, for example, regulat...
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Veröffentlicht in: | The American journal of the medical sciences 2013-05, Vol.345 (5), p.401-404 |
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description | Abstract Acute stressor states are inextricably linked to neurohormonal activation which includes the adrenergic nervous system. Consequent elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K+ , Mg2+ and Ca2+ . Catecholamines, for example, regulate the large number of Mg2+ -dependent Na/K ATPase pumps present in skeletal muscle. A hyperadrenergic state accounts for a sudden translocation of K+ into muscle and rapid appearance of hypokalemia. In the myocardium, catecholamines promote Mg2+ efflux from cardiomyocytes, whereas intracellular Ca2+ influx and overloading account for the induction of oxidative stress and necrosis of these cells with leakage of their contents, including troponins. Accordingly, acute stressor states can be accompanied by nonischemic elevations in serum troponins, together with the concordant appearance of hypokalemia, hypomagnesemia and ionized hypocalcemia, causing a delay in myocardial repolarization and electrocardiographic QTc prolongation raising the propensity for arrhythmias, including atrial fibrillation and polymorphic ventricular tachycardia. In this review, we focus on the interdependency between K+ , Mg2+ and Ca2+ which are clinically relevant to acute stressor states. |
doi_str_mv | 10.1097/MAJ.0b013e318253cb07 |
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Consequent elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K+ , Mg2+ and Ca2+ . Catecholamines, for example, regulate the large number of Mg2+ -dependent Na/K ATPase pumps present in skeletal muscle. A hyperadrenergic state accounts for a sudden translocation of K+ into muscle and rapid appearance of hypokalemia. In the myocardium, catecholamines promote Mg2+ efflux from cardiomyocytes, whereas intracellular Ca2+ influx and overloading account for the induction of oxidative stress and necrosis of these cells with leakage of their contents, including troponins. Accordingly, acute stressor states can be accompanied by nonischemic elevations in serum troponins, together with the concordant appearance of hypokalemia, hypomagnesemia and ionized hypocalcemia, causing a delay in myocardial repolarization and electrocardiographic QTc prolongation raising the propensity for arrhythmias, including atrial fibrillation and polymorphic ventricular tachycardia. In this review, we focus on the interdependency between K+ , Mg2+ and Ca2+ which are clinically relevant to acute stressor states.</description><identifier>ISSN: 0002-9629</identifier><identifier>EISSN: 1538-2990</identifier><identifier>DOI: 10.1097/MAJ.0b013e318253cb07</identifier><identifier>PMID: 22739557</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acute Disease ; Animals ; Calcium - blood ; Catecholamines ; Catecholamines - blood ; Elevated troponins ; Humans ; Internal Medicine ; Ionized calcium ; Magnesium ; Magnesium - blood ; Nonischemic necrosis ; Parathyroid hormone ; Potassium ; Potassium - blood ; Stress, Physiological - physiology ; Stress, Psychological - blood ; Stress, Psychological - diagnosis</subject><ispartof>The American journal of the medical sciences, 2013-05, Vol.345 (5), p.401-404</ispartof><rights>Southern Society for Clinical Investigation</rights><rights>2012 Southern Society for Clinical Investigation</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-41cf848cba947d0236aa86a8e73f437f6bd5a048e5908ffefe30db075f1071e23</citedby><cites>FETCH-LOGICAL-c417t-41cf848cba947d0236aa86a8e73f437f6bd5a048e5908ffefe30db075f1071e23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27931,27932</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22739557$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Weber, Karl T.</contributor><creatorcontrib>Usman Khan, M., MD</creatorcontrib><creatorcontrib>Komolafe, Babatunde O., MD</creatorcontrib><creatorcontrib>Weber, Karl T., MD</creatorcontrib><title>Cation Interdependency in Acute Stressor States</title><title>The American journal of the medical sciences</title><addtitle>Am J Med Sci</addtitle><description>Abstract Acute stressor states are inextricably linked to neurohormonal activation which includes the adrenergic nervous system. Consequent elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K+ , Mg2+ and Ca2+ . Catecholamines, for example, regulate the large number of Mg2+ -dependent Na/K ATPase pumps present in skeletal muscle. A hyperadrenergic state accounts for a sudden translocation of K+ into muscle and rapid appearance of hypokalemia. In the myocardium, catecholamines promote Mg2+ efflux from cardiomyocytes, whereas intracellular Ca2+ influx and overloading account for the induction of oxidative stress and necrosis of these cells with leakage of their contents, including troponins. Accordingly, acute stressor states can be accompanied by nonischemic elevations in serum troponins, together with the concordant appearance of hypokalemia, hypomagnesemia and ionized hypocalcemia, causing a delay in myocardial repolarization and electrocardiographic QTc prolongation raising the propensity for arrhythmias, including atrial fibrillation and polymorphic ventricular tachycardia. In this review, we focus on the interdependency between K+ , Mg2+ and Ca2+ which are clinically relevant to acute stressor states.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Calcium - blood</subject><subject>Catecholamines</subject><subject>Catecholamines - blood</subject><subject>Elevated troponins</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Ionized calcium</subject><subject>Magnesium</subject><subject>Magnesium - blood</subject><subject>Nonischemic necrosis</subject><subject>Parathyroid hormone</subject><subject>Potassium</subject><subject>Potassium - blood</subject><subject>Stress, Physiological - physiology</subject><subject>Stress, Psychological - blood</subject><subject>Stress, Psychological - diagnosis</subject><issn>0002-9629</issn><issn>1538-2990</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtPwzAQhC0EgvL4Bwj1yCWwfiS2L0hVxVNFHICz5ThryZAmxU6Q-u9xVeDAhdPuYXZH8w0hpxQuKGh5-Th7uIAaKEdOFSu5q0HukAktuSqY1rBLJgDACl0xfUAOU3oDoExRvk8OGJNcl6WckMu5HULfTe-7AWODK-wa7Nx6GrrpzI0DTp-HiCn1MS92wHRM9rxtE558zyPyenP9Mr8rFk-39_PZonCCyqEQ1HkllKutFrIBxitrVWUVSu4Fl76qm9KCUFhqUN6jRw5NDlB6CpIi40fkfPt3FfuPEdNgliE5bFvbYT8mQzmnoISueJaKrdTFPqWI3qxiWNq4NhTMBpXJqMxfVPns7NthrJfY_B79sMmCq60Ac87PgNEkFzIcbEJEN5imD_85_H3g2tAFZ9t3XGN668fYZYaGmsQMmOdNXZu2coVQVVLwLyVujWc</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Usman Khan, M., MD</creator><creator>Komolafe, Babatunde O., MD</creator><creator>Weber, Karl T., MD</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20130501</creationdate><title>Cation Interdependency in Acute Stressor States</title><author>Usman Khan, M., MD ; Komolafe, Babatunde O., MD ; Weber, Karl T., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-41cf848cba947d0236aa86a8e73f437f6bd5a048e5908ffefe30db075f1071e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Calcium - blood</topic><topic>Catecholamines</topic><topic>Catecholamines - blood</topic><topic>Elevated troponins</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Ionized calcium</topic><topic>Magnesium</topic><topic>Magnesium - blood</topic><topic>Nonischemic necrosis</topic><topic>Parathyroid hormone</topic><topic>Potassium</topic><topic>Potassium - blood</topic><topic>Stress, Physiological - physiology</topic><topic>Stress, Psychological - blood</topic><topic>Stress, Psychological - diagnosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Usman Khan, M., MD</creatorcontrib><creatorcontrib>Komolafe, Babatunde O., MD</creatorcontrib><creatorcontrib>Weber, Karl T., MD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The American journal of the medical sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Usman Khan, M., MD</au><au>Komolafe, Babatunde O., MD</au><au>Weber, Karl T., MD</au><au>Weber, Karl T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cation Interdependency in Acute Stressor States</atitle><jtitle>The American journal of the medical sciences</jtitle><addtitle>Am J Med Sci</addtitle><date>2013-05-01</date><risdate>2013</risdate><volume>345</volume><issue>5</issue><spage>401</spage><epage>404</epage><pages>401-404</pages><issn>0002-9629</issn><eissn>1538-2990</eissn><abstract>Abstract Acute stressor states are inextricably linked to neurohormonal activation which includes the adrenergic nervous system. Consequent elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K+ , Mg2+ and Ca2+ . Catecholamines, for example, regulate the large number of Mg2+ -dependent Na/K ATPase pumps present in skeletal muscle. A hyperadrenergic state accounts for a sudden translocation of K+ into muscle and rapid appearance of hypokalemia. In the myocardium, catecholamines promote Mg2+ efflux from cardiomyocytes, whereas intracellular Ca2+ influx and overloading account for the induction of oxidative stress and necrosis of these cells with leakage of their contents, including troponins. Accordingly, acute stressor states can be accompanied by nonischemic elevations in serum troponins, together with the concordant appearance of hypokalemia, hypomagnesemia and ionized hypocalcemia, causing a delay in myocardial repolarization and electrocardiographic QTc prolongation raising the propensity for arrhythmias, including atrial fibrillation and polymorphic ventricular tachycardia. In this review, we focus on the interdependency between K+ , Mg2+ and Ca2+ which are clinically relevant to acute stressor states.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22739557</pmid><doi>10.1097/MAJ.0b013e318253cb07</doi><tpages>4</tpages></addata></record> |
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subjects | Acute Disease Animals Calcium - blood Catecholamines Catecholamines - blood Elevated troponins Humans Internal Medicine Ionized calcium Magnesium Magnesium - blood Nonischemic necrosis Parathyroid hormone Potassium Potassium - blood Stress, Physiological - physiology Stress, Psychological - blood Stress, Psychological - diagnosis |
title | Cation Interdependency in Acute Stressor States |
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