The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function - Tabular View

Tracking Information
First Received Date ^ICMJE	November 3, 1999
Last Updated Date	March 3, 2008
Start Date ^ICMJE	July 1997
Primary Completion Date
Current Primary Outcome Measures ^ICMJE
Original Primary Outcome Measures ^ICMJE
Change History	Complete list of historical versions of study NCT00001628 on ClinicalTrials.gov Archive Site
Current Secondary Outcome Measures ^ICMJE
Original Secondary Outcome Measures ^ICMJE

Descriptive Information
Brief Title ^ICMJE	The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function
Official Title ^ICMJE	The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function
Brief Summary	The renin angiotensin system (RAS) plays an important physiological and pathophysiological role in the control of blood pressure and plasma volume. Inhibition of the RAS is useful in the treatment of hypertension, cardiac failure and in some patients with myocardial infarction. Several recent clinical trials with angiotensin converting enzyme inhibitors (ACEI) have shown that they also reduce the incidence of myocardial infarction, but the mechanisms underlying this anti-ischemic effect are poorly understood. ACEI reduce angiotensin II synthesis and prevent bradykinin degradation. Results from ongoing studies in the Cardiology Branch (Protocol 95-H-0099) designed to investigate the link between ACEI and the vascular endothelium indicate that ACEI improve peripheral endothelial function, an effect that is partially mediated by bradykinin. The current protocol is designed to investigate whether the beneficial effects of ACEI on peripheral endothelial function are also due to inhibition of angiotensin II. The recent development of selective angiotensin II type 1 (AT1) receptor antagonists allows us to specifically examine the effects of angiotensin II on vasomotor activity.
Detailed Description	The renin angiotensin system (RAS) plays an important physiological and pathophysiological role in the control of blood pressure and plasma volume. Inhibition of the RAS is useful in the treatment of hypertension, cardiac failure and in some patients with myocardial infarction. Several recent clinical trials with angiotensin converting enzyme inhibitors (ACEI) have shown that they also reduce the incidence of myocardial infarction, but the mechanisms underlying this anti-ischemic effect are poorly understood. ACEI reduce angiotensin II synthesis and prevent bradykinin degradation. Results from ongoing studies in the Cardiology Branch (Protocol 95-H-0099) designed to investigate the link between ACEI and the vascular endothelium indicate that ACEI improve peripheral endothelial function, an effect that is partially mediated by bradykinin. The current protocol is designed to investigate whether the beneficial effects of ACEI on peripheral endothelial function are also due to inhibition of angiotensin II. The recent development of selective angiotensin II type 1 (AT1) receptor antagonists allows us to specifically examine the effects of angiotensin II on vasomotor activity.
Study Phase	Phase III
Study Type ^ICMJE	Interventional
Study Design ^ICMJE	Treatment, Efficacy Study
Condition ^ICMJE	Atherosclerosis Heart Failure, Congestive Hypertension Myocardial Infarction
Intervention ^ICMJE	Drug: Angiotensin II type 1 receptor antagonists
Study Arms / Comparison Groups
Publications *	Ontyd J, Schrader J. Measurement of adenosine, inosine, and hypoxanthine in human plasma. J Chromatogr. 1984 May 11;307(2):404-9. No abstract available. Cockcroft JR, Sciberras DG, Goldberg MR, Ritter JM. Comparison of angiotensin-converting enzyme inhibition with angiotensin II receptor antagonism in the human forearm. J Cardiovasc Pharmacol. 1993 Oct;22(4):579-84. Gottlieb SS, Dickstein K, Fleck E, Kostis J, Levine TB, LeJemtel T, DeKock M. Hemodynamic and neurohormonal effects of the angiotensin II antagonist losartan in patients with congestive heart failure. Circulation. 1993 Oct;88(4 Pt 1):1602-9.
* Includes publications given by the data provider as well as publications identified by National Clinical Trials Identifier (NCT ID) in Medline.

Recruitment Information
Recruitment Status ^ICMJE	Completed
Enrollment ^ICMJE	36
Completion Date	September 2000
Primary Completion Date
Eligibility Criteria ^ICMJE	Patients over 18 years with endothelial dysfunction requiring diagnostic cardiac catheterization. Normal volunteers or patients undergoing catheterization who have normal coronary arteries without risk factors for atherosclerosis will be used as controls. No unstable angina. No significant left main disease (greater than 50% stenosis). No recent myocardial infarction (less than 1 month). No pregnancy, lactation. No allergy to losartan. No renal failure (creatinine greater than 2.5 mg/dl). Ability to withdraw ACE inhibitors.
Gender	Both
Ages
Accepts Healthy Volunteers	Yes
Contacts ^ICMJE	Contact information is only displayed when the study is recruiting subjects
Location Countries ^ICMJE	United States

Administrative Information
NCT ID ^ICMJE	NCT00001628
Responsible Party
Study ID Numbers ^ICMJE	970140, 97-H-0140
Study Sponsor ^ICMJE	National Heart, Lung, and Blood Institute (NHLBI)
Collaborators ^ICMJE
Investigators ^ICMJE
Information Provided By	National Institutes of Health Clinical Center (CC)
Verification Date	June 1999
^ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP