ИСТИНА

Aim. Acidosis induces arterial relaxation, but its effects on endothelium are purely understood. We have shown earlier that NO exerts a powerful anticontractile effects and mediates a half of acetylcholine (ACh)-induced relaxation in murine basilar artery (BA). This study was aimed at the effects of acidosis on NO-ergic control of BA. Methods. BA segments from male C57BL/6 mice were mounted in wire myograph. NO effects were studied using L-NNA, given either alone or after blockade of other endothelial pathways by the combination of indomethacin, TRAM-34 and UCL-1684. Extracellular acidosis was induced by bubbling the solution with 10% CO2 in O2 (instead of 5% CO2 under control conditions). Results. Contractile responses of BA to U46619 were suppressed by acidosis. However, under both control and acidic conditions L-NNA prominently increased maximum force and the sensitivity to U46619 (5-10-fold decrease of EC50), while the combination of other blockers did not potentiate the contraction. Relaxation of BA to ACh (after U46619-precontraction) was slightly reduced by acidosis but demonstrated a paradoxical increase of NO-component along with strongly depressed contribution of other pathways. L-NNA halved the response under control conditions but reduced it by 90% in acidified BA; the combined effect of other blockers under acidosis was negligible. NO-sensitivity of BA (studied by relaxation to DEA-NO) was increased by acidosis as well. Conclusions. Acidosis did not affect anticontractile influence of NO. However, it strongly potentiated NO effects during activation of the endothelium, which may be important for vasomotor control under acidification of brain milieu.