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| Sponsored by: |
National Heart, Lung, and Blood Institute (NHLBI) |
| Information provided by: | National Institutes of Health Clinical Center (CC) |
| ClinicalTrials.gov Identifier: | NCT00001628 |
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 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.
| Condition | Intervention | Phase |
|
Atherosclerosis Heart Failure, Congestive Hypertension Myocardial Infarction |
Drug: Angiotensin II type 1 receptor antagonists |
Phase III |
| MedlinePlus related topics: | Heart Attack Heart Failure High Blood Pressure |
| Drug Information available for: | Angiotensin II Angiotensin II, ile(5)- |
| Study Type: | Interventional |
| Study Design: | Treatment, Efficacy Study |
| Official Title: | The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function |
| Estimated Enrollment: | 36 |
| Study Start Date: | July 1997 |
| Estimated Study Completion Date: | September 2000 |
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.
Eligibility
| Genders Eligible for Study: | Both |
| Accepts Healthy Volunteers: | Yes |
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.
Contacts and Locations More Information
| Study ID Numbers: | 970140, 97-H-0140 |
| First Received: | November 3, 1999 |
| Last Updated: | March 3, 2008 |
| ClinicalTrials.gov Identifier: | NCT00001628 |
| Health Authority: | United States: Federal Government |
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