EFFECTS OF NITRIC-OXIDE AND SODIUM-NITROPRUSSIDE ON THE INTRINSIC ELASTIC PROPERTIES OF PRESSURIZED RAT CORONARY-ARTERY

The study was designed to assess the influence of either nitric oxide (NO) or sodium nitroprusside and the absence of endothelium on the int rinsic elastic properties of coronary arteries from WKY rats. For this purpose, segments of the right interventricular coronary were mounted in an arteriograph where wall thickness and internal diameter were co ntinuously monitored while intraluminal pressure was controlled in the absence of flow. To study the passive properties, pressure-diameter r elationships were determined by measuring the corresponding internal d iameter for each stepwise increase in intraluminal pressure. Thus, wal l stress, strain and incremental elastic modulus (E(inc)) were assesse d in the following experimental conditions: control, incubation with n itro-L-arginine methyl ester(L-NAME, 100 mu M) or L-NAME + L-arginine (L-arg, 100 mu M), incubation with sodium nitroprusside (SNP, 100 mu M ), endothelium removal (CHAPS). The E(inc)-stress relationship was not significantly different in the different experimental conditions, but values of E(inc) plotted as function of strain were significantly dec reased after L-NAME incubation and partly reversed after L-arg additio n. The same effect was observed after endothelium destruction but to a lesser extent. After SNP incubation, values of E(inc) were significan tly decreased for small values of strain and increased for high values of this parameter. These results show that NO synthase inhibition ind uced, for a given strain, a decrease of elastic modulus in coronary ar teries. It can be speculated that functional antagonism exerted by NO against spontaneous contractile tone was reduced. Thus, the smooth mus cle cells were in a greater state of activation and probably more stro ngly involved in the intrinsic elastic properties of this preparation. However, an unexplained effect of NO on wall stiffness cannot be excl uded. Conversely, SNP increased the initial diameter and induced an in itial decrease in stiffness followed by a subsequent increase. After e ndothelium destruction, stiffness was significantly decreased compared to control conditions. It can be concluded that NO modulates the intr insic elastic properties of the coronary arteries through smooth muscl e cell relaxation. Furthermore, results with SNP support the hypothesi s that the lower the state of activation of the smooth muscle cells, t he higher the elastic modulus of the arterial wall in this coronary ar tery preparation.