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The Role of Angiotensin Type I Receptor in the Regulation of Human Coronary Vascular Function

This study has been completed.
Sponsor:
ClinicalTrials.gov Identifier:
NCT00001629
First Posted: December 10, 2002
Last Update Posted: March 4, 2008
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Information provided by:
National Institutes of Health Clinical Center (CC)
  Purpose
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 both endothelial dysfunction and metabolic coronary vasodilation, an effect that is partially mediated by bradykinin. The current protocol is designed to investigate whether the beneficial effects of ACEI on endothelial function are also partly 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.

Condition Intervention Phase
Atherosclerosis Heart Failure, Congestive Hypertension Myocardial Infarction Drug: Angiotensin II type 1 receptor antagonists Phase 3

Study Type: Interventional
Study Design: Primary Purpose: Treatment
Official Title: The Role of Angiotensin Type I Receptor in the Regulation of Human Coronary Vascular Function

Further study details as provided by National Institutes of Health Clinical Center (CC):

Estimated Enrollment: 49
Study Start Date: July 1997
Estimated Study Completion Date: September 2000
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 both endothelial dysfunction and metabolic coronary vasodilation, an effect that is partially mediated by bradykinin. The current protocol is designed to investigate whether the beneficial effects of ACEI on endothelial function are also partly 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.
  Eligibility

Information from the National Library of Medicine

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Ages Eligible for Study:   Child, Adult, Senior
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Criteria

Patient must be over 18 years of age requiring diagnostic cardiac catheterization will participate.

Women on chronic estrogen therapy are eligible for the study.

Patients investigated for chest pain syndrome with normal coronary arteries with and without risk factors for atherosclerosis, patients with coronary artery disease, and patients with heart failure.

No patients with unstable angina; significant left main disease (greater than 50% stenosis); Recent myocardial infarction (less than 1 month); Pregnancy, lactation; Allergy to losartan; Renal failure (creatinine greater than 2.5 mg/dl); Inability to withdraw ACE inhibitors.

  Contacts and Locations
Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00001629


Locations
United States, Maryland
National Heart, Lung and Blood Institute (NHLBI)
Bethesda, Maryland, United States, 20892
Sponsors and Collaborators
National Heart, Lung, and Blood Institute (NHLBI)
  More Information

Publications:
ClinicalTrials.gov Identifier: NCT00001629     History of Changes
Other Study ID Numbers: 970142
97-H-0142
First Submitted: November 3, 1999
First Posted: December 10, 2002
Last Update Posted: March 4, 2008
Last Verified: June 1999

Keywords provided by National Institutes of Health Clinical Center (CC):
Angiotensin AT-1 Receptor
Angiotensin Receptor Antagonist
Atherosclerosis
Blood Flow
Cold Pressor Test
Endothelium
Exercise
Coronary Artery Disease
Heart Failure

Additional relevant MeSH terms:
Heart Failure
Infarction
Myocardial Infarction
Atherosclerosis
Heart Diseases
Cardiovascular Diseases
Ischemia
Pathologic Processes
Necrosis
Myocardial Ischemia
Vascular Diseases
Arteriosclerosis
Arterial Occlusive Diseases
Angiotensin II
Angiotensinogen
Angiotensin Receptor Antagonists
Angiotensin II Type 1 Receptor Blockers
Vasoconstrictor Agents
Serine Proteinase Inhibitors
Protease Inhibitors
Enzyme Inhibitors
Molecular Mechanisms of Pharmacological Action