Nctid:
NCT00001527
Payload:
{"FullStudy"=>{"Rank"=>497876, "Study"=>{"DerivedSection"=>{"MiscInfoModule"=>{"VersionHolder"=>"June 24, 2024"}, "ConditionBrowseModule"=>{"ConditionMeshList"=>{"ConditionMesh"=>[{"ConditionMeshId"=>"D000006973", "ConditionMeshTerm"=>"Hypertension"}, {"ConditionMeshId"=>"D000075222", "ConditionMeshTerm"=>"Essential Hypertension"}]}, "ConditionAncestorList"=>{"ConditionAncestor"=>[{"ConditionAncestorId"=>"D000014652", "ConditionAncestorTerm"=>"Vascular Diseases"}, {"ConditionAncestorId"=>"D000002318", "ConditionAncestorTerm"=>"Cardiovascular Diseases"}]}, "ConditionBrowseLeafList"=>{"ConditionBrowseLeaf"=>[{"ConditionBrowseLeafId"=>"M10024", "ConditionBrowseLeafName"=>"Hypertension", "ConditionBrowseLeafAsFound"=>"Hypertension", "ConditionBrowseLeafRelevance"=>"high"}, {"ConditionBrowseLeafId"=>"M1470", "ConditionBrowseLeafName"=>"Essential Hypertension", "ConditionBrowseLeafAsFound"=>"Essential Hypertension", "ConditionBrowseLeafRelevance"=>"high"}, {"ConditionBrowseLeafId"=>"M17400", "ConditionBrowseLeafName"=>"Vascular Diseases", "ConditionBrowseLeafRelevance"=>"low"}]}, "ConditionBrowseBranchList"=>{"ConditionBrowseBranch"=>[{"ConditionBrowseBranchName"=>"Heart and Blood Diseases", "ConditionBrowseBranchAbbrev"=>"BC14"}, {"ConditionBrowseBranchName"=>"All Conditions", "ConditionBrowseBranchAbbrev"=>"All"}]}}, "InterventionBrowseModule"=>{"InterventionBrowseLeafList"=>{"InterventionBrowseLeaf"=>[{"InterventionBrowseLeafId"=>"M255666", "InterventionBrowseLeafName"=>"cyclo(Trp-Asp-Pro-Val-Leu)", "InterventionBrowseLeafRelevance"=>"low"}, {"InterventionBrowseLeafId"=>"M244726", "InterventionBrowseLeafName"=>"BQ 788", "InterventionBrowseLeafRelevance"=>"low"}]}, "InterventionBrowseBranchList"=>{"InterventionBrowseBranch"=>[{"InterventionBrowseBranchName"=>"Antihypertensive Agents", "InterventionBrowseBranchAbbrev"=>"AnAg"}, {"InterventionBrowseBranchName"=>"All Drugs and Chemicals", "InterventionBrowseBranchAbbrev"=>"All"}]}}}, "ProtocolSection"=>{"DesignModule"=>{"StudyType"=>"Observational", "EnrollmentInfo"=>{"EnrollmentCount"=>"60"}}, "StatusModule"=>{"OverallStatus"=>"Completed", "StartDateStruct"=>{"StartDate"=>"November 1995"}, "ExpandedAccessInfo"=>{"HasExpandedAccess"=>"No"}, "StatusVerifiedDate"=>"November 1999", "CompletionDateStruct"=>{"CompletionDate"=>"September 2000"}, "LastUpdateSubmitDate"=>"March 3, 2008", "StudyFirstSubmitDate"=>"November 3, 1999", "StudyFirstSubmitQCDate"=>"December 9, 2002", "LastUpdatePostDateStruct"=>{"LastUpdatePostDate"=>"March 4, 2008", "LastUpdatePostDateType"=>"Estimate"}, "StudyFirstPostDateStruct"=>{"StudyFirstPostDate"=>"December 10, 2002", "StudyFirstPostDateType"=>"Estimate"}}, "OversightModule"=>{}, "ConditionsModule"=>{"KeywordList"=>{"Keyword"=>["BQ-123", "BQ-788", "Endothelin", "Endothelium", "Plethysmography", "Essential Hypertension"]}, "ConditionList"=>{"Condition"=>["Hypertension"]}}, "ReferencesModule"=>{"ReferenceList"=>{"Reference"=>[{"ReferencePMID"=>"2451132", "ReferenceType"=>"background", "ReferenceCitation"=>"Yanagisawa M, Kurihara H, Kimura S, Tomobe Y, Kobayashi M, Mitsui Y, Yazaki Y, Goto K, Masaki T. A novel potent vasoconstrictor peptide produced by vascular endothelial cells. Nature. 1988 Mar 31;332(6163):411-5. doi: 10.1038/332411a0."}, {"ReferencePMID"=>"7831383", "ReferenceType"=>"background", "ReferenceCitation"=>"Rubanyi GM, Polokoff MA. Endothelins: molecular biology, biochemistry, pharmacology, physiology, and pathophysiology. Pharmacol Rev. 1994 Sep;46(3):325-415. No abstract available."}, {"ReferencePMID"=>"2175397", "ReferenceType"=>"background", "ReferenceCitation"=>"Sakurai T, Yanagisawa M, Takuwa Y, Miyazaki H, Kimura S, Goto K, Masaki T. Cloning of a cDNA encoding a non-isopeptide-selective subtype of the endothelin receptor. Nature. 1990 Dec 20-27;348(6303):732-5. doi: 10.1038/348732a0."}]}}, "DescriptionModule"=>{"BriefSummary"=>"Endothelin-1 (ET-1) is a powerful vasoconstricting peptide produced predominantly by vascular endothelial cells, that exerts its effect through the interaction with specific receptors, ETA and ETB, on the underlying smooth muscle cells. Previous studies in normal subjects have demonstrated an increase in forearm blood flow after ET-1 antagonism, suggesting a physiologic role of ET-1 in the regulation of basal vascular tone. However, whether ET-1-mediated tone is increased in hypertensive patients is unknown.\n\nThe main purpose of this study will be to compare the forearm vascular responses to local infusion of ET-1 receptor antagonists between normotensive and hypertensive subjects in order to assess whether ET-1-mediated basal tone is increased in patients with hypertension. In addition, we propose to study the vascular responses to local ET-1 infusion to determine whether vascular smooth muscle sensitivity to this peptide is increased in hypertensive vessels. We will use both an ETA receptor antagonist, BQ-123, and an ETB receptor antagonist, BQ-788, in order to evaluate the relative contribution of the two receptor subtypes to the regulation of vascular tone.\n\nAll drugs will be infused into the brachial artery and the responses of the forearm vasculature will be measured by means of strain gauge plethysmography. Because of the relative long-lasting effect of most of the substances to be infused, the study will be performed on two separate occasions.", "DetailedDescription"=>"Endothelin-1 (ET-1) is a powerful vasoconstricting peptide produced predominantly by vascular endothelial cells, that exerts its effect through the interaction with specific receptors, ETA and ETB, on the underlying smooth muscle cells. Previous studies in normal subjects have demonstrated an increase in forearm blood flow after ET-1 antagonism, suggesting a physiologic role of ET-1 in the regulation of basal vascular tone. However, whether ET-1-mediated tone is increased in hypertensive patients is unknown.\n\nThe main purpose of this study will be to compare the forearm vascular responses to local infusion of ET-1 receptor antagonists between normotensive and hypertensive subjects in order to assess whether ET-1-mediated basal tone is increased in patients with hypertension. In addition, we propose to study the vascular responses to local ET-1 infusion to determine whether vascular smooth muscle sensitivity to this peptide is increased in hypertensive vessels. We will use both an ETA receptor antagonist, BQ-123, and an ETB receptor antagonist, BQ-788, in order to evaluate the relative contribution of the two receptor subtypes to the regulation of vascular tone.\n\nAll drugs will be infused into the brachial artery and the responses of the forearm vasculature will be measured by means of strain gauge plethysmography. Because of the relative long-lasting effect of most of the substances to be infused, the study will be performed on two separate occasions."}, "EligibilityModule"=>{"Gender"=>"All", "StdAgeList"=>{"StdAge"=>["Child", "Adult", "Older Adult"]}, "HealthyVolunteers"=>"Accepts Healthy Volunteers", "EligibilityCriteria"=>"Between 40-65 years old.\n\nNormal Volunteers who are not taking medications. Have no medical problems. Cholesterol below 200 mg/dl. No contraceptives.\n\nHypertensive Patients with blood pressure greater than 145/90 off medications. Serum cholesterol less than 200 mg/dl. No other medical problems.\n\nHigh cholesterol patients with cholesterol level greater than 250 mg/dl. No other medical problems."}, "IdentificationModule"=>{"NCTId"=>"NCT00001527", "BriefTitle"=>"Role of Endothelin in the Regulation of Vascular Tone in Patients With Essential Hypertension", "Organization"=>{"OrgClass"=>"NIH", "OrgFullName"=>"National Institutes of Health Clinical Center (CC)"}, "OfficialTitle"=>"Role of Endothelin in the Regulation of Vascular Tone in Patients With Essential Hypertension", "OrgStudyIdInfo"=>{"OrgStudyId"=>"960016"}, "SecondaryIdInfoList"=>{"SecondaryIdInfo"=>[{"SecondaryId"=>"96-H-0016"}]}}, "ContactsLocationsModule"=>{"LocationList"=>{"Location"=>[{"LocationZip"=>"20892", "LocationCity"=>"Bethesda", "LocationState"=>"Maryland", "LocationCountry"=>"United States", "LocationFacility"=>"National Heart, Lung and Blood Institute (NHLBI)"}]}}, "SponsorCollaboratorsModule"=>{"LeadSponsor"=>{"LeadSponsorName"=>"National Heart, Lung, and Blood Institute (NHLBI)", "LeadSponsorClass"=>"NIH"}}}}}}
