{"title":"Drinking and vasopressin release following central injections of angiotensin II in minipigs.","authors":"S N Thornton, M L Forsling, B A Baldwin","doi":"10.1113/expphysiol.1989.sp003257","DOIUrl":null,"url":null,"abstract":"<p><p>Angiotensin II (AII; 300 ng) injected into the lateral cerebral ventricle produced significant drinking responses and also stimulated release of lysine vasopressin (LVP) in conscious, water replete, unrestrained minipigs. Plasma LVP concentration, measured by a specific radioimmunoassay, was decreased by drinking. At the end of the experiment the level was inversely proportional to the volume of water drunk in response to the AII, and not to changes in plasma osmolality. These findings suggest that AII-stimulated LVP release is influenced by a negative feed-back mechanism, probably involving oropharyngeal receptors.</p>","PeriodicalId":77774,"journal":{"name":"Quarterly journal of experimental physiology (Cambridge, England)","volume":"74 2","pages":"211-4"},"PeriodicalIF":0.0000,"publicationDate":"1989-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1113/expphysiol.1989.sp003257","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Quarterly journal of experimental physiology (Cambridge, England)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1113/expphysiol.1989.sp003257","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Angiotensin II (AII; 300 ng) injected into the lateral cerebral ventricle produced significant drinking responses and also stimulated release of lysine vasopressin (LVP) in conscious, water replete, unrestrained minipigs. Plasma LVP concentration, measured by a specific radioimmunoassay, was decreased by drinking. At the end of the experiment the level was inversely proportional to the volume of water drunk in response to the AII, and not to changes in plasma osmolality. These findings suggest that AII-stimulated LVP release is influenced by a negative feed-back mechanism, probably involving oropharyngeal receptors.