[Effect of N-Nitro-L-Arginine on the concentration and relaxation of vascular smooth muscle]

Abstract

The arterial smooth muscle contractility is regulated by the free intracellular calcium concentration and by alpha 1 and alpha 2 adrenergic receptor stimulation (norepinephrine (NE), phenylephrine (PHE) and clonidine), inducing contraction, increase in vascular tension and increase in intracellular calcium concentration. This response is increased in the absence of endothelium. On the other hand, the relaxation of isolated arteries induced by acetylcholine (ACh) is endothelium-dependent and modulate by EDRF. We have studied the effect of pre incubation with N-nitro-L-arginine (L-NA) on the alpha-adrenergic-induced-contraction and ACh-induced relaxation, respectively in isolated rat toraxic aorta strips in comparison with the effect produced by 70 mM KCl which is taken as control. The results show a significant difference (p < 0.001) in the presence of L-NA on the PHE-induced contraction compared to the absence of L-NA. At the three ACh concentration used, the presence of L-NA induced relaxation less than 20%. The absence of L-NA produced 100% relaxation returning to base line. L-NA induces an increase in calcium entry through receptor modulated calcium channels, and because the inhibition of the synthesis of EDRF it would produce an increase in vascular tension. In the same way, relaxation is explained by ACh-stimulated EDRF release, which is inhibited by L-NA. Considering the vascular endothelium as a paracrine organ, is important and interesting to study the pharmacomodulation of the NO/EDRF effects and, for the same reason, to consider L-NA in the pharmacologic arsenal.