Central administration of angiotensin II receptor antagonists and arterial pressure regulation: A note of caution
The blunting of arterial pressure increases to a variety of pressor agents or the lowering of arterial pressure in some models of hypertension following intracerebroventricular administration of an angiotensin II (AII) antagonist, has been interpreted as prima facie evidence for the involvement of t...
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| Veröffentlicht in: | Life sciences (1973) 1992, Vol.50 (20), p.1497-1502 |
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| creator | Gruber, Kenneth A. Callahan, Michael F. Eskridge-Sloop, Shawnee L. |
| description | The blunting of arterial pressure increases to a variety of pressor agents or the lowering of arterial pressure in some models of hypertension following intracerebroventricular administration of an angiotensin II (AII) antagonist, has been interpreted as
prima facie
evidence for the involvement of the central AII system in these situations.
Central administration of vasopressin or carbachol (a cholinergic agonist) produces pressor effects which have been reported to be due to an increase in the activity of the sympathetic nervous system. We now report that central administration of AII antagonists [either (Sar-1, Ile-8) AII or (Sar-1, Ala-8) AII] in rats prevents the majority (>70%) of the pressor effects of intraventricular vasopressin or carbachol.
These results can be interpreted in two ways. The first is that all of these pressor agents use a central angiotensinergic mechanism(s) to increase sympathetic nervous system activity. An alternative hypothesis is that centrally administered AII antagonists non-specifically inhibit sympathetic nervous system function. |
| doi_str_mv | 10.1016/0024-3205(92)90139-G |
| format | Article |
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prima facie
evidence for the involvement of the central AII system in these situations.
Central administration of vasopressin or carbachol (a cholinergic agonist) produces pressor effects which have been reported to be due to an increase in the activity of the sympathetic nervous system. We now report that central administration of AII antagonists [either (Sar-1, Ile-8) AII or (Sar-1, Ala-8) AII] in rats prevents the majority (>70%) of the pressor effects of intraventricular vasopressin or carbachol.
These results can be interpreted in two ways. The first is that all of these pressor agents use a central angiotensinergic mechanism(s) to increase sympathetic nervous system activity. An alternative hypothesis is that centrally administered AII antagonists non-specifically inhibit sympathetic nervous system function.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/0024-3205(92)90139-G</identifier><identifier>PMID: 1579044</identifier><identifier>CODEN: LIFSAK</identifier><language>eng</language><publisher>OXFORD: Elsevier Inc</publisher><subject>1-Sarcosine-8-Isoleucine Angiotensin II - pharmacology ; Angiotensin Receptor Antagonists ; Animals ; Biological and medical sciences ; Blood Pressure ; Carbachol - pharmacology ; Fundamental and applied biological sciences. Psychology ; Hemodynamics. Rheology ; Life Sciences & Biomedicine ; Medicine, Research & Experimental ; Pharmacology & Pharmacy ; Rats ; Rats, Inbred Strains ; Research & Experimental Medicine ; Saralasin - pharmacology ; Science & Technology ; Vasopressins - pharmacology ; Vertebrates: cardiovascular system</subject><ispartof>Life sciences (1973), 1992, Vol.50 (20), p.1497-1502</ispartof><rights>1992</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>8</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wosA1992HN74800004</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c417t-ab09b7e889ad1351eab5adfb6ce9a91f03479960bbcbbcb1c36bbb46b9b72a203</citedby><cites>FETCH-LOGICAL-c417t-ab09b7e889ad1351eab5adfb6ce9a91f03479960bbcbbcb1c36bbb46b9b72a203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0024-3205(92)90139-G$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,4025,27197,27928,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4537896$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1579044$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gruber, Kenneth A.</creatorcontrib><creatorcontrib>Callahan, Michael F.</creatorcontrib><creatorcontrib>Eskridge-Sloop, Shawnee L.</creatorcontrib><title>Central administration of angiotensin II receptor antagonists and arterial pressure regulation: A note of caution</title><title>Life sciences (1973)</title><addtitle>LIFE SCI</addtitle><addtitle>Life Sci</addtitle><description>The blunting of arterial pressure increases to a variety of pressor agents or the lowering of arterial pressure in some models of hypertension following intracerebroventricular administration of an angiotensin II (AII) antagonist, has been interpreted as
prima facie
evidence for the involvement of the central AII system in these situations.
Central administration of vasopressin or carbachol (a cholinergic agonist) produces pressor effects which have been reported to be due to an increase in the activity of the sympathetic nervous system. We now report that central administration of AII antagonists [either (Sar-1, Ile-8) AII or (Sar-1, Ala-8) AII] in rats prevents the majority (>70%) of the pressor effects of intraventricular vasopressin or carbachol.
These results can be interpreted in two ways. The first is that all of these pressor agents use a central angiotensinergic mechanism(s) to increase sympathetic nervous system activity. An alternative hypothesis is that centrally administered AII antagonists non-specifically inhibit sympathetic nervous system function.</description><subject>1-Sarcosine-8-Isoleucine Angiotensin II - pharmacology</subject><subject>Angiotensin Receptor Antagonists</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Carbachol - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hemodynamics. Rheology</subject><subject>Life Sciences & Biomedicine</subject><subject>Medicine, Research & Experimental</subject><subject>Pharmacology & Pharmacy</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Research & Experimental Medicine</subject><subject>Saralasin - pharmacology</subject><subject>Science & Technology</subject><subject>Vasopressins - pharmacology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EZCTM</sourceid><sourceid>EIF</sourceid><recordid>eNqNkluLFDEQhYMo67j6DxT6QURZWnPrS_ZhYWh0dmDRF30OSbp6iPQks0la8d9venoY31whkKLqOwdSJwi9JvgjwaT-hDHlJaO4ei_oB4EJE-XmCVqRthElrhl5ilZn5Dl6EeNPjHFVNewCXZCqEZjzFbrvwKWgxkL1e-tszHWy3hV-KJTbWZ_AReuK7bYIYOCQfMj9pHZ-ZmOu-0KFBMFmi0OAGKcAGd1N49HnulgXLpvMfkZNc-slejaoMcKr032Jfnz5_L27Le--bbbd-q40nDSpVBoL3UDbCtUTVhFQulL9oGsDQgkyYMYbIWqstZkPMazWWvNaZxVVFLNL9G7xPQR_P0FMcm-jgXFUDvwUZUMFoy3jj4KkplgQRjLIF9AEH2OAQR6C3avwRxIs50jkvG8571sKKo-RyE2WvTn5T3oP_V_RkkGevz3NVTRqHIJyxsYzxivWtKLOWLtgv0H7IRoLzsCZWhMh6O3Xhrc5ZMw7m4777_zkUpZe_b800zcLDTmdXxaCPCl6m_9Akr23_37wA97Oy0E</recordid><startdate>1992</startdate><enddate>1992</enddate><creator>Gruber, Kenneth A.</creator><creator>Callahan, Michael F.</creator><creator>Eskridge-Sloop, Shawnee L.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>BLEPL</scope><scope>DTL</scope><scope>EZCTM</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>1992</creationdate><title>Central administration of angiotensin II receptor antagonists and arterial pressure regulation: A note of caution</title><author>Gruber, Kenneth A. ; Callahan, Michael F. ; Eskridge-Sloop, Shawnee L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-ab09b7e889ad1351eab5adfb6ce9a91f03479960bbcbbcb1c36bbb46b9b72a203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>1-Sarcosine-8-Isoleucine Angiotensin II - pharmacology</topic><topic>Angiotensin Receptor Antagonists</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Carbachol - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hemodynamics. Rheology</topic><topic>Life Sciences & Biomedicine</topic><topic>Medicine, Research & Experimental</topic><topic>Pharmacology & Pharmacy</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Research & Experimental Medicine</topic><topic>Saralasin - pharmacology</topic><topic>Science & Technology</topic><topic>Vasopressins - pharmacology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gruber, Kenneth A.</creatorcontrib><creatorcontrib>Callahan, Michael F.</creatorcontrib><creatorcontrib>Eskridge-Sloop, Shawnee L.</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 1992</collection><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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gruber, Kenneth A.</au><au>Callahan, Michael F.</au><au>Eskridge-Sloop, Shawnee L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Central administration of angiotensin II receptor antagonists and arterial pressure regulation: A note of caution</atitle><jtitle>Life sciences (1973)</jtitle><stitle>LIFE SCI</stitle><addtitle>Life Sci</addtitle><date>1992</date><risdate>1992</risdate><volume>50</volume><issue>20</issue><spage>1497</spage><epage>1502</epage><pages>1497-1502</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><coden>LIFSAK</coden><abstract>The blunting of arterial pressure increases to a variety of pressor agents or the lowering of arterial pressure in some models of hypertension following intracerebroventricular administration of an angiotensin II (AII) antagonist, has been interpreted as
prima facie
evidence for the involvement of the central AII system in these situations.
Central administration of vasopressin or carbachol (a cholinergic agonist) produces pressor effects which have been reported to be due to an increase in the activity of the sympathetic nervous system. We now report that central administration of AII antagonists [either (Sar-1, Ile-8) AII or (Sar-1, Ala-8) AII] in rats prevents the majority (>70%) of the pressor effects of intraventricular vasopressin or carbachol.
These results can be interpreted in two ways. The first is that all of these pressor agents use a central angiotensinergic mechanism(s) to increase sympathetic nervous system activity. An alternative hypothesis is that centrally administered AII antagonists non-specifically inhibit sympathetic nervous system function.</abstract><cop>OXFORD</cop><pub>Elsevier Inc</pub><pmid>1579044</pmid><doi>10.1016/0024-3205(92)90139-G</doi><tpages>6</tpages></addata></record> |
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| source | Web of Science - Science Citation Index Expanded - 1992<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | 1-Sarcosine-8-Isoleucine Angiotensin II - pharmacology Angiotensin Receptor Antagonists Animals Biological and medical sciences Blood Pressure Carbachol - pharmacology Fundamental and applied biological sciences. Psychology Hemodynamics. Rheology Life Sciences & Biomedicine Medicine, Research & Experimental Pharmacology & Pharmacy Rats Rats, Inbred Strains Research & Experimental Medicine Saralasin - pharmacology Science & Technology Vasopressins - pharmacology Vertebrates: cardiovascular system |
| title | Central administration of angiotensin II receptor antagonists and arterial pressure regulation: A note of caution |
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