Hormonal Responses and Blood Pressure Maintenance in Normal and Hypertensive Subjects During Acute Blood Loss
Blood pressure (BP) and plasma indices of three major pressure control systems – plasma norepinephrine and epinephrine, plasma renin activity (PRA), and plasma arginine vasopressin – were measured simultaneously in 12 normal and 15 mildly essential hypertensive subjects before and after removal of 4...
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Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 1987-05, Vol.9 (5), p.423-428 |
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description | Blood pressure (BP) and plasma indices of three major pressure control systems – plasma norepinephrine and epinephrine, plasma renin activity (PRA), and plasma arginine vasopressin – were measured simultaneously in 12 normal and 15 mildly essential hypertensive subjects before and after removal of 480 ml of blood by phlebotomy, to determine if there were differences in the compensatory response to acute blood loss. Responses to postural stress (change from supine to sitting position) following phlebotomy were also compared in a second group of subjects. Before phlebotomy, supine plasma hormone levels did not differ in the two groups. After phlebotomy, both groups exhibited only slight decreases (5 mm Hg) in systolic BP and a transient rise in heart rate. Only plasma norepinephrine increased significantly in both groups (35% above control in normal and 43% hi hypertensive subjects). Similar results were obtained in a second group of normal and hypertensive subjects, who were also subjected to a 10-minute postural challenge after phlebotomy. After 10 minutes in a sitting position, BP in these subjects remained unchanged but heart rate and plasma norepinephrine increased further to levels almost twice that produced by phlebotomy alone. Plasma epinephrine levels and PRA also increased with this additional stress, but plasma vasopressin remained unchanged. Changes in BP, heart rate, plasma norepinephrine and epinephrine, and PRA did not differ significantly between the two groups. These data indicate that 1) hypertensive subjects are as capable as normal subjects of maintaining BP when subjected to standard phlebotomy, 2) the sympathetic nervous system appears to be the predominant pressor mechanism activated following an acute, nonhypotensive blood loss in both groups of subjects, and 3) the addition of postural stress further accentuates the sympathetic response and increases PRA. |
doi_str_mv | 10.1161/01.HYP.9.5.423 |
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Responses to postural stress (change from supine to sitting position) following phlebotomy were also compared in a second group of subjects. Before phlebotomy, supine plasma hormone levels did not differ in the two groups. After phlebotomy, both groups exhibited only slight decreases (5 mm Hg) in systolic BP and a transient rise in heart rate. Only plasma norepinephrine increased significantly in both groups (35% above control in normal and 43% hi hypertensive subjects). Similar results were obtained in a second group of normal and hypertensive subjects, who were also subjected to a 10-minute postural challenge after phlebotomy. After 10 minutes in a sitting position, BP in these subjects remained unchanged but heart rate and plasma norepinephrine increased further to levels almost twice that produced by phlebotomy alone. Plasma epinephrine levels and PRA also increased with this additional stress, but plasma vasopressin remained unchanged. Changes in BP, heart rate, plasma norepinephrine and epinephrine, and PRA did not differ significantly between the two groups. These data indicate that 1) hypertensive subjects are as capable as normal subjects of maintaining BP when subjected to standard phlebotomy, 2) the sympathetic nervous system appears to be the predominant pressor mechanism activated following an acute, nonhypotensive blood loss in both groups of subjects, and 3) the addition of postural stress further accentuates the sympathetic response and increases PRA.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.9.5.423</identifier><identifier>PMID: 3552977</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Adult ; Arginine Vasopressin - blood ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Blood Volume ; Bloodletting ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Epinephrine - blood ; Female ; Heart Rate ; Hormones - blood ; Humans ; Hypertension - blood ; Hypertension - physiopathology ; Male ; Medical sciences ; Middle Aged ; Norepinephrine - blood ; Potassium - blood ; Renin - blood ; Sodium - blood</subject><ispartof>Hypertension (Dallas, Tex. 1979), 1987-05, Vol.9 (5), p.423-428</ispartof><rights>1987 American Heart Association, Inc.</rights><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4441-cbf4632dc23012feda4cad18fce7d8d28712648e7dd14efb09a7d290efc30df3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7476372$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3552977$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VELASQUEZ, MANUEL T</creatorcontrib><creatorcontrib>MENTTOVE, JAY E</creatorcontrib><creatorcontrib>SKELTON, MEREDITH M</creatorcontrib><creatorcontrib>COWLEY, ALLEN W</creatorcontrib><title>Hormonal Responses and Blood Pressure Maintenance in Normal and Hypertensive Subjects During Acute Blood Loss</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Blood pressure (BP) and plasma indices of three major pressure control systems – plasma norepinephrine and epinephrine, plasma renin activity (PRA), and plasma arginine vasopressin – were measured simultaneously in 12 normal and 15 mildly essential hypertensive subjects before and after removal of 480 ml of blood by phlebotomy, to determine if there were differences in the compensatory response to acute blood loss. Responses to postural stress (change from supine to sitting position) following phlebotomy were also compared in a second group of subjects. Before phlebotomy, supine plasma hormone levels did not differ in the two groups. After phlebotomy, both groups exhibited only slight decreases (5 mm Hg) in systolic BP and a transient rise in heart rate. Only plasma norepinephrine increased significantly in both groups (35% above control in normal and 43% hi hypertensive subjects). Similar results were obtained in a second group of normal and hypertensive subjects, who were also subjected to a 10-minute postural challenge after phlebotomy. After 10 minutes in a sitting position, BP in these subjects remained unchanged but heart rate and plasma norepinephrine increased further to levels almost twice that produced by phlebotomy alone. Plasma epinephrine levels and PRA also increased with this additional stress, but plasma vasopressin remained unchanged. Changes in BP, heart rate, plasma norepinephrine and epinephrine, and PRA did not differ significantly between the two groups. These data indicate that 1) hypertensive subjects are as capable as normal subjects of maintaining BP when subjected to standard phlebotomy, 2) the sympathetic nervous system appears to be the predominant pressor mechanism activated following an acute, nonhypotensive blood loss in both groups of subjects, and 3) the addition of postural stress further accentuates the sympathetic response and increases PRA.</description><subject>Adult</subject><subject>Arginine Vasopressin - blood</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure</subject><subject>Blood Volume</subject><subject>Bloodletting</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Epinephrine - blood</subject><subject>Female</subject><subject>Heart Rate</subject><subject>Hormones - blood</subject><subject>Humans</subject><subject>Hypertension - blood</subject><subject>Hypertension - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Norepinephrine - blood</subject><subject>Potassium - blood</subject><subject>Renin - blood</subject><subject>Sodium - blood</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kM1v1DAQxS0EKkvhyg3JB8QtweM4cXws5WORFqigBzhZXntCUxJn8SRU_e_xaqP6Yo3f7z2PHmMvQZQADbwVUG5_XZWmrEslq0dsA7VUhaqb6jHbCDCqMAA_n7JnRLdCgFJKn7Gzqq6l0XrDxu2Uxim6gX9HOkyRkLiLgb8bpinwq4RES0L-xfVxxuiiR95H_jWbsuUIbu8PmLJE_T_kP5b9LfqZ-Psl9fE3v_DLjGvWbiJ6zp50biB8sd7n7Prjh-vLbbH79unz5cWu8Hk_KPy-U00lg5eVANlhcMq7AG3nUYc2yFaDbFSbhwAKu70wTgdpBHa-EqGrztmbU-whTX8XpNmOPXkcBhdxWshqrVohjMxgeQJ9ytsl7Owh9aNL9xaEPdZrBdhcrzW2trnebHi1Ji_7EcMDvvaZ9der7si7oUu5sZ4eMK10U-njv-qE3U3DjIn-DMsdJnuDbphvrMhHyaYtwLRa1Hkqjk9Q_QckipPc</recordid><startdate>198705</startdate><enddate>198705</enddate><creator>VELASQUEZ, MANUEL T</creator><creator>MENTTOVE, JAY E</creator><creator>SKELTON, MEREDITH M</creator><creator>COWLEY, ALLEN W</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><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>198705</creationdate><title>Hormonal Responses and Blood Pressure Maintenance in Normal and Hypertensive Subjects During Acute Blood Loss</title><author>VELASQUEZ, MANUEL T ; MENTTOVE, JAY E ; SKELTON, MEREDITH M ; COWLEY, ALLEN W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4441-cbf4632dc23012feda4cad18fce7d8d28712648e7dd14efb09a7d290efc30df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Adult</topic><topic>Arginine Vasopressin - blood</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure</topic><topic>Blood Volume</topic><topic>Bloodletting</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Epinephrine - blood</topic><topic>Female</topic><topic>Heart Rate</topic><topic>Hormones - blood</topic><topic>Humans</topic><topic>Hypertension - blood</topic><topic>Hypertension - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Norepinephrine - blood</topic><topic>Potassium - blood</topic><topic>Renin - blood</topic><topic>Sodium - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VELASQUEZ, MANUEL T</creatorcontrib><creatorcontrib>MENTTOVE, JAY E</creatorcontrib><creatorcontrib>SKELTON, MEREDITH M</creatorcontrib><creatorcontrib>COWLEY, ALLEN W</creatorcontrib><collection>Pascal-Francis</collection><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>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VELASQUEZ, MANUEL T</au><au>MENTTOVE, JAY E</au><au>SKELTON, MEREDITH M</au><au>COWLEY, ALLEN W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hormonal Responses and Blood Pressure Maintenance in Normal and Hypertensive Subjects During Acute Blood Loss</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>1987-05</date><risdate>1987</risdate><volume>9</volume><issue>5</issue><spage>423</spage><epage>428</epage><pages>423-428</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Blood pressure (BP) and plasma indices of three major pressure control systems – plasma norepinephrine and epinephrine, plasma renin activity (PRA), and plasma arginine vasopressin – were measured simultaneously in 12 normal and 15 mildly essential hypertensive subjects before and after removal of 480 ml of blood by phlebotomy, to determine if there were differences in the compensatory response to acute blood loss. Responses to postural stress (change from supine to sitting position) following phlebotomy were also compared in a second group of subjects. Before phlebotomy, supine plasma hormone levels did not differ in the two groups. After phlebotomy, both groups exhibited only slight decreases (5 mm Hg) in systolic BP and a transient rise in heart rate. Only plasma norepinephrine increased significantly in both groups (35% above control in normal and 43% hi hypertensive subjects). Similar results were obtained in a second group of normal and hypertensive subjects, who were also subjected to a 10-minute postural challenge after phlebotomy. After 10 minutes in a sitting position, BP in these subjects remained unchanged but heart rate and plasma norepinephrine increased further to levels almost twice that produced by phlebotomy alone. Plasma epinephrine levels and PRA also increased with this additional stress, but plasma vasopressin remained unchanged. Changes in BP, heart rate, plasma norepinephrine and epinephrine, and PRA did not differ significantly between the two groups. These data indicate that 1) hypertensive subjects are as capable as normal subjects of maintaining BP when subjected to standard phlebotomy, 2) the sympathetic nervous system appears to be the predominant pressor mechanism activated following an acute, nonhypotensive blood loss in both groups of subjects, and 3) the addition of postural stress further accentuates the sympathetic response and increases PRA.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>3552977</pmid><doi>10.1161/01.HYP.9.5.423</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Arginine Vasopressin - blood Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure Blood Volume Bloodletting Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Epinephrine - blood Female Heart Rate Hormones - blood Humans Hypertension - blood Hypertension - physiopathology Male Medical sciences Middle Aged Norepinephrine - blood Potassium - blood Renin - blood Sodium - blood |
title | Hormonal Responses and Blood Pressure Maintenance in Normal and Hypertensive Subjects During Acute Blood Loss |
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