Vasopressin as a possible contributor to hypertension
The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment....
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Veröffentlicht in: | Japanese circulation journal 1984-01, Vol.48 (2), p.188-195 |
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container_title | Japanese circulation journal |
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creator | Yazaki, Y Ohuchi, Y Ashida, T Tsai, R Yoshizumi, M |
description | The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. However, the role of vasopressin remains to be determined in human essential hypertension. |
doi_str_mv | 10.1253/jcj.48.188 |
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Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. However, the role of vasopressin remains to be determined in human essential hypertension.</description><identifier>ISSN: 0047-1828</identifier><identifier>EISSN: 1347-4839</identifier><identifier>DOI: 10.1253/jcj.48.188</identifier><identifier>PMID: 6321816</identifier><language>eng</language><publisher>Japan</publisher><subject>Animals ; Blood Pressure - drug effects ; Chlorides - pharmacology ; Deamino Arginine Vasopressin - pharmacology ; Desoxycorticosterone - pharmacology ; Hypertension - chemically induced ; Hypertension - etiology ; Hypertension - physiopathology ; Injections, Intravenous ; Lithium - pharmacology ; Lithium Chloride ; Male ; Rats ; Receptors, Angiotensin - physiology ; Salts ; Vasopressins - pharmacology ; Vasopressins - physiology</subject><ispartof>Japanese circulation journal, 1984-01, Vol.48 (2), p.188-195</ispartof><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-1ab8e3cbd6bace737df8ba23eca7ebb3ae4193bda2db56219c1c2afc8db328c23</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6321816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yazaki, Y</creatorcontrib><creatorcontrib>Ohuchi, Y</creatorcontrib><creatorcontrib>Ashida, T</creatorcontrib><creatorcontrib>Tsai, R</creatorcontrib><creatorcontrib>Yoshizumi, M</creatorcontrib><title>Vasopressin as a possible contributor to hypertension</title><title>Japanese circulation journal</title><addtitle>Jpn Circ J</addtitle><description>The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. However, the role of vasopressin remains to be determined in human essential hypertension.</description><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>Chlorides - pharmacology</subject><subject>Deamino Arginine Vasopressin - pharmacology</subject><subject>Desoxycorticosterone - pharmacology</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - etiology</subject><subject>Hypertension - physiopathology</subject><subject>Injections, Intravenous</subject><subject>Lithium - pharmacology</subject><subject>Lithium Chloride</subject><subject>Male</subject><subject>Rats</subject><subject>Receptors, Angiotensin - physiology</subject><subject>Salts</subject><subject>Vasopressins - pharmacology</subject><subject>Vasopressins - physiology</subject><issn>0047-1828</issn><issn>1347-4839</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9j0tLw0AUhQdRaq1u3AuzFhLnziO5WUqxKhTcqNthXsGENgkz6aL_3pEWV-csPg7nI-QeWAlciafe9aXEEhAvyBKErAuJorkkS8ZyB-R4TW5S6hnjtVRqQRaV4IBQLYn6NmmcYkipG6hJ1NBpzN3uAnXjMMfOHuYx0nmkP8cpxDkMqRuHW3LVml0Kd-dcka_Ny-f6rdh-vL6vn7eFk6jmAozFIJz1lTUu1KL2LVrDRXCmDtYKEyQ0wnrDvVUVh8aB46Z16K3g6LhYkcfTrov5VQytnmK3N_Gogek_dZ3VtUSd1TP8cIKng90H_4-eXcUvaWZWgQ</recordid><startdate>19840101</startdate><enddate>19840101</enddate><creator>Yazaki, Y</creator><creator>Ohuchi, Y</creator><creator>Ashida, T</creator><creator>Tsai, R</creator><creator>Yoshizumi, M</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>19840101</creationdate><title>Vasopressin as a possible contributor to hypertension</title><author>Yazaki, Y ; Ohuchi, Y ; Ashida, T ; Tsai, R ; Yoshizumi, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-1ab8e3cbd6bace737df8ba23eca7ebb3ae4193bda2db56219c1c2afc8db328c23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>Chlorides - pharmacology</topic><topic>Deamino Arginine Vasopressin - pharmacology</topic><topic>Desoxycorticosterone - pharmacology</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - etiology</topic><topic>Hypertension - physiopathology</topic><topic>Injections, Intravenous</topic><topic>Lithium - pharmacology</topic><topic>Lithium Chloride</topic><topic>Male</topic><topic>Rats</topic><topic>Receptors, Angiotensin - physiology</topic><topic>Salts</topic><topic>Vasopressins - pharmacology</topic><topic>Vasopressins - physiology</topic><toplevel>online_resources</toplevel><creatorcontrib>Yazaki, Y</creatorcontrib><creatorcontrib>Ohuchi, Y</creatorcontrib><creatorcontrib>Ashida, T</creatorcontrib><creatorcontrib>Tsai, R</creatorcontrib><creatorcontrib>Yoshizumi, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Japanese circulation journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yazaki, Y</au><au>Ohuchi, Y</au><au>Ashida, T</au><au>Tsai, R</au><au>Yoshizumi, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vasopressin as a possible contributor to hypertension</atitle><jtitle>Japanese circulation journal</jtitle><addtitle>Jpn Circ J</addtitle><date>1984-01-01</date><risdate>1984</risdate><volume>48</volume><issue>2</issue><spage>188</spage><epage>195</epage><pages>188-195</pages><issn>0047-1828</issn><eissn>1347-4839</eissn><abstract>The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. 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subjects | Animals Blood Pressure - drug effects Chlorides - pharmacology Deamino Arginine Vasopressin - pharmacology Desoxycorticosterone - pharmacology Hypertension - chemically induced Hypertension - etiology Hypertension - physiopathology Injections, Intravenous Lithium - pharmacology Lithium Chloride Male Rats Receptors, Angiotensin - physiology Salts Vasopressins - pharmacology Vasopressins - physiology |
title | Vasopressin as a possible contributor to hypertension |
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