Blockade of EDRF synthesis with NG-nitro-L-arginine methyl ester reduces acetylcholine-induced vasodilation and enhances noradrenaline-induced vasoconstriction in the rabbit inferior vena cava.
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No immediate clinical implications; confirms EDRF/NO mediation of acetylcholine and noradrenaline responses in rabbit veins.
Endothelium-derived relaxing factor (EDRF) has been shown to influence arterial tone, but controversial results have been obtained studying veins. The present study was performed to determine the importance of EDRF for the inferior vena cava in the rabbit and whether blockade of the synthesis of EDRF with NG-nitro-L-arginine methyl ester may influence the reactivity of the inferior vena cava to noradrenaline. 2. The inferior vena cava was excised in six New Zealand white rabbits and 12 rings were prepared for organ bath studies. Concentration-response curves were constructed for acetylcholine (10(-9)-10(-4) mol/L) and noradrenaline (10(-9)-10(-4) mol/L) before and following the administration of NG-nitro-L-arginine methyl ester. 3. All rings showed concentration-dependent relaxation to acetylcholine (mean maximum: 57 +/- 9%) following precontraction with noradrenaline (EC50:10(-6) mol/L). Following NG-nitro-L-arginine methyl ester, this dilation was significantly reduced to a mean maximum relaxation of 13 +/- 6% (P < 0.01). 4. Contraction of the inferior vena cava to increasing doses of noradrenaline reached a maximum of 5.8 +/- 2.8 g before NG-nitro-L-arginine methyl ester (basal tension 1.0 +/- 0.5 g). NG-nitro-L-arginine methyl ester did not affect basal tension, but the constrictor response to noradrenaline was enhanced significantly to a maximum of 9.1 +/- 3.8 g (P < 0.01). 5. Although it cannot be ascertained definitively from the present results, it is suggested that EDRF is mediating vasodilation of the inferior vena cava and that this vasoactive agent may also contributes significantly to the modulation of the reactivity to catecholamines.
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Schwarzacher et al. (1996) studied this question.
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