Contribution of bradykinin receptor dysfunction to abnormal coronary vasomotion in humans
- 25 October 2000
- journal article
- Published by Elsevier in Journal of the American College of Cardiology
- Vol. 36 (5), 1467-1473
- https://doi.org/10.1016/s0735-1097(00)00892-5
Abstract
No abstract availableKeywords
This publication has 26 references indexed in Scilit:
- Abnormal flow-mediated epicardial vasomotion in human coronary arteries is improved by angiotensin-converting enzyme inhibition: A potential role of bradykininJournal of the American College of Cardiology, 1999
- Bradykinin-Induced Vasodilation of Human Coronary Arteries In Vivo: Role of Nitric Oxide and Angiotensin-Converting EnzymeJournal of the American College of Cardiology, 1997
- Role of Endogenous Bradykinin in Human Coronary Vasomotor ControlCirculation, 1995
- Contribution of Nitric Oxide to Metabolic Coronary Vasodilation in the Human HeartCirculation, 1995
- Nitric oxide activity in the human coronary circulation. Impact of risk factors for coronary atherosclerosis.Journal of Clinical Investigation, 1995
- Inhibition of bradykinin‐induced vasodilation in human forearm vasculature by icatibant, a potent B2‐receptor antagonist.British Journal of Clinical Pharmacology, 1994
- Endothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries.Journal of Clinical Investigation, 1993
- An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels.Journal of Clinical Investigation, 1990
- Paradoxical Vasoconstriction Induced by Acetylcholine in Atherosclerotic Coronary ArteriesNew England Journal of Medicine, 1986
- Effect of vasoactive peptides on prostacyclin synthesis in manBritish Journal of Pharmacology, 1986