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Home > "T" Clinical Trials Conditions > The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function  The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function
The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function
For Condition: Atherosclerosis,Heart Failure, Congestive,Hypertension,Myocardial Infarction
Status: Completed
Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) ,
Synopsis: 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.
Details: 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:
Study Type: Interventional, Treatment, Efficacy
Minimum Age/Maximum Age: /
Genders: Both
Protocol Entry 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.
Total Enrollment: 36
Location and Contact Information:
National Heart, Lung and Blood Institute (NHLBI)
Bethesda, Maryland, 20892
United States
Additional Information:
Study ID Numbers: 970140; 97-H-0140
Study Start Date: July 1, 1997
Record last reviewed: June 16, 1999
Additional information available at: clinicaltrials.gov
Clinicaltrials.gov Reference link: NCT00001628
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4. Genetic Architecture of Plasma T-PA and PAI-1
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The Role of Angiotensin Type I Receptor in the Regulation of Human Peripheral Vascular Function
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