Abstract
The following clinical summaries serve to illustrate a hypothesis for a mechanism for the development and treatment of tolerance to NTG. Whereas previous efforts to explain and treat tolerance have centered on enzymatic conversion of NTG to NO in the vascular smooth muscle cell, we present and discuss evidence that points to L-arginine depletion as a defect that leads to the development of tolerance to NTG. It appears that pharmacologic supplementation of nitrates with L-arginine may be a means for reversing, treating, and possibly preventing nitrate tolerance. Clinical trials to examine the impact of this approach on endpoints currently missing in the treatment of unstable angina and myocardial infarction seem warranted.
Original language | English (US) |
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Pages (from-to) | 255-262 |
Number of pages | 8 |
Journal | Applied Cardiopulmonary Pathophysiology |
Volume | 6 |
Issue number | 4 |
State | Published - 1996 |
Keywords
- L-arginine
- Myocardial infarction
- Nitrate tolerance
- Nitric oxide
- Organic nitrates
- Unstable angina
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Cardiology and Cardiovascular Medicine
- Physiology (medical)