New insights into mechanisms underlying nitrate tolerance.

[1]  T. Münzel,et al.  Long-term angiotensin-converting enzyme inhibition with high-dose enalapril retards nitrate tolerance in large epicardial arteries and prevents rebound coronary vasoconstriction in vivo. , 1996, Circulation.

[2]  D. Harrison,et al.  Dissociation of coronary vascular tolerance and neurohormonal adjustments during long-term nitroglycerin therapy in patients with stable coronary artery disease. , 1996, Journal of the American College of Cardiology.

[3]  H. Drexler,et al.  Absence of vascular tolerance in conductance vessels after 48 hours of intravenous nitroglycerin in patients with coronary artery disease. , 1995, Journal of the American College of Cardiology.

[4]  B. Fink,et al.  Vitamin C and other antioxidants suppress nitrate-induced tolerance , 1995 .

[5]  D. Harrison,et al.  Evidence for enhanced vascular superoxide anion production in nitrate tolerance. A novel mechanism underlying tolerance and cross-tolerance. , 1995, The Journal of clinical investigation.

[6]  E. Ohlstein,et al.  Angiotensin type 1 receptors mediate smooth muscle proliferation and endothelin biosynthesis in rat vascular smooth muscle. , 1994, The Journal of pharmacology and experimental therapeutics.

[7]  R W Alexander,et al.  Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. , 1994, Circulation research.

[8]  S. Loft,et al.  Nitrate tolerance in vivo is not associated with depletion of arterial or venous thiol levels. , 1994, Circulation research.

[9]  V. Breu,et al.  Downregulation of endothelin receptors by autocrine production of endothelin-1. , 1993, The American journal of physiology.

[10]  D. Stewart,et al.  Expression of endothelin-1 in the lungs of patients with pulmonary hypertension. , 1993, The New England journal of medicine.

[11]  J. Parker,et al.  Effect of therapy with an angiotensin-converting enzyme inhibitor on hemodynamic and counterregulatory responses during continuous therapy with nitroglycerin. , 1993, Journal of the American College of Cardiology.

[12]  M. Walsh,et al.  Protein kinase C of smooth muscle. , 1992, Hypertension.

[13]  J. Parker,et al.  Counter‐Regulatory Responses to Continuous and Intermittent Therapy With Nitroglycerin , 1991, Circulation.

[14]  M. Kelm,et al.  Biotransformation of organic nitrates to nitric oxide by vascular smooth muscle and endothelial cells. , 1991, Biochemical and biophysical research communications.

[15]  A. Lerman,et al.  Circulating and tissue endothelin immunoreactivity in advanced atherosclerosis. , 1991, The New England journal of medicine.

[16]  K. Schrör,et al.  Reduced Nitric Oxide Release Causes Nitrate Tolerance in the Intact Coronary Circulation , 1991, Journal of cardiovascular pharmacology.

[17]  U. Elkayam Tolerance to organic nitrates: evidence, mechanisms, clinical relevance, and strategies for prevention. , 1991, Annals of internal medicine.

[18]  J. Rouleau,et al.  Tolerance to intravenous nitroglycerin in patients with congestive heart failure: role of increased intravascular volume, neurohumoral activation and lack of prevention with N-acetylcysteine. , 1990, Journal of the American College of Cardiology.

[19]  T. Resink,et al.  Stimulation of endothelin mRNA and secretion in rat vascular smooth muscle cells: a novel autocrine function. , 1990, Cell regulation.

[20]  J. Brien,et al.  Biotransformation of glyceryl trinitrate and isosorbide dinitrate in vascular smooth muscle made tolerant to organic nitrates. , 1989, Canadian journal of physiology and pharmacology.

[21]  D. Stewart,et al.  Nitrate tolerance in epicardial arteries or in the venous system is not reversed by N-acetylcysteine in vivo, but tolerance-independent interactions exist. , 1989, Circulation.

[22]  N. Reichek,et al.  Antianginal effects of intravenous nitroglycerin over 24 hours. , 1988, Circulation.

[23]  H. Fung,et al.  Mechanisms for the pharmacologic interaction of organic nitrates with thiols. Existence of an extracellular pathway for the reversal of nitrate vascular tolerance by N-acetylcysteine. , 1988, The Journal of pharmacology and experimental therapeutics.

[24]  J. Abrams A reappraisal of nitrate therapy. , 1988, JAMA.

[25]  C. McKay,et al.  Hemodynamic and volumetric effects of venodilation with nitroglycerin in chronic mitral regurgitation. , 1987, The American journal of cardiology.

[26]  M. Feelisch,et al.  Nitric oxide (NO) formation from nitrovasodilators occurs independently of hemoglobin or non-heme iron. , 1987, European journal of pharmacology.

[27]  F. Murad,et al.  Effect of In Vivo Nitroglycerin Therapy on Endothelium‐Dependent and Independent Vascular Relaxation and Cyclic GMP Accumulation in Rat Aorta , 1987, Journal of cardiovascular pharmacology.

[28]  S. Gottlieb,et al.  Prevention and reversal of nitrate tolerance in patients with congestive heart failure. , 1987, The New England journal of medicine.

[29]  W. Hsueh,et al.  Incidence of early tolerance to hemodynamic effects of continuous infusion of nitroglycerin in patients with coronary artery disease and heart failure. , 1987, Circulation.

[30]  S. Moncada,et al.  Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor , 1987, Nature.

[31]  F. Murad,et al.  Desensitization to nitroglycerin in vascular smooth muscle from rat and human. , 1986, Biochemical pharmacology.

[32]  D. Stewart,et al.  Altered spectrum of nitroglycerin action in long-term treatment: nitroglycerin-specific venous tolerance with maintenance of arterial vasodepressor potency. , 1986, Circulation.

[33]  R. Andersson,et al.  Tolerance towards nitroglycerin, induced in vivo, is correlated to a reduced cGMP response and an alteration in cGMP turnover. , 1983, European journal of pharmacology.

[34]  P. Needleman,et al.  Mechanism of tolerance development to organic nitrates. , 1973, The Journal of pharmacology and experimental therapeutics.