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

National Institutes of Health (NIH) logo

National Institutes of Health (NIH)

Status and phase

Completed
Phase 3

Conditions

Hypertension
Heart Failure, Congestive
Myocardial Infarction
Atherosclerosis

Treatments

Drug: Angiotensin II type 1 receptor antagonists

Study type

Interventional

Funder types

NIH

Identifiers

NCT00001628
97-H-0140
970140

Details and patient eligibility

About

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.

Full 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.

Sex

All

Volunteers

Accepts Healthy Volunteers

Inclusion and exclusion criteria

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.

Trial contacts and locations

1

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Data sourced from clinicaltrials.gov

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