Extracellular acidosis promote endothelium‐independent and nitric oxide‐dependent vasodilation

Abstract

Extracellular acidosis (EA) has profound effects on vascular homeostasis since EA‐induced tone alterations are specific to vascular bed. In the present study, we examined the in vitro ("organ chambers") effects of acidosis on dilatory responses of isolated rat thoracic aorta. pH‐response curves (7.4 to 6.5) were generated using HCl (1M) in phenylephrine pre‐contracted endothelium intact and denuded rings. The acidosis pH‐response curves were obtained by gradual addition of HCl to the preparation. The curves were performed with and without tetraethylamonium (TEA), NG‐nitro‐L‐arginina metil ester (L‐NAME) and/or indomethacin (Indo). Relaxation mediated by HCl was increased in endothelium intact rings (73.12±3.66) compared to denuded rings (39.56±3.78) during mild (pH 7.0), but not severe acidosis (pH 6.5) (94.33±1.96 to 91.42±0.95). Mild acidosis‐dilatory effect in endothelium intact rings was markedly reduced by L‐NAME (32.54±5.38) and L‐NAME + Indo (22.80±7.36). In denuded rings, relaxation was reduced only by L‐NAME in mild (11.52±4.18) and in severe acidosis (53.32±6.44). TEA and Indo failed to alter the relaxing effect of acidosis. These results point that acidosis promoted nitric oxide (NO)‐mediated relaxation in rat aorta. Moreover, other factors, besides NO, can be involved in relaxation mediated by EA. Support: FAPESP; FAEPA‐HC/FMRP.