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L-NAME enhances pulmonary vasoconstriction without inhibiting EDRF-dependent vasodilation
1Department of Internal Medicine, Louisiana State University Medical School, New Orleans.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|December 1, 1992
Summary
NG-nitro-L-arginine methyl ester (L-NAME) affects pulmonary vascular responses. L-NAME inhibits serotonin-induced vasodilation by enhancing serotonin2 receptor-mediated vasoconstriction, not by inhibiting EDRF formation.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Endothelium-dependent relaxing factor (EDRF) plays a crucial role in regulating pulmonary vascular tone.
- NG-nitro-L-arginine methyl ester (L-NAME) is a commonly used inhibitor of EDRF synthesis.
- Understanding L-NAME's specific effects in the pulmonary vasculature is essential for interpreting experimental data.
Purpose of the Study:
- To investigate the impact of L-NAME on pulmonary vascular responses to both EDRF-dependent and EDRF-independent vasoactive agents in anesthetized cats.
- To elucidate the mechanism by which L-NAME influences pulmonary vasodilation and vasoconstriction.
Main Methods:
- Anesthetized cats were used, with controlled pulmonary blood flow and left atrial pressure to isolate changes in pulmonary vascular resistance.
- Pulmonary vasomotor tone was modulated using U-46619, followed by intralobar injections of acetylcholine, bradykinin, serotonin, and 5-carboxyamidotryptamine.
- The effects of L-NAME administration were assessed on vasodilator responses and vasoconstrictor responses to a serotonin2 receptor agonist, with interventions using ritanserin and L-arginine.
Main Results:
- L-NAME significantly attenuated the pulmonary vasodilator response to serotonin but not to 5-carboxyamidotryptamine, acetylcholine, or bradykinin.
- Administration of ritanserin reversed L-NAME's inhibitory effect on serotonin-induced vasodilation and abolished enhanced vasoconstriction to a serotonin2 receptor agonist.
- L-arginine did not reverse the inhibitory effects of L-NAME.
Conclusions:
- L-NAME inhibits pulmonary vasodilator responses to serotonin primarily by increasing serotonin2 receptor-mediated vasoconstriction sensitivity, rather than by inhibiting EDRF formation.
- The lack of inhibition of acetylcholine and bradykinin responses by L-NAME suggests it may not be a reliable tool for studying endogenous EDRF in the feline pulmonary vasculature in vivo.