ACIDOSIS IMPAIRS RABBIT TRABECULAR SMOOTH-MUSCLE CONTRACTILITY

Purpose. The aim of our study was to define the effects of acidosis on the contractility of trabecular smooth muscle. Methods. Rabbit corpus cavernosal strips were mounted in organ chambers to measure isometric tension. Additionally, intracellular free Ca2+ concentration ([Ca2+]( i)) and tension were measured simultaneously utilising the intracellul ar fluorescent dye, FURA-2, and isometric tension recordings. Results. Contraction of corpus cavernosum smooth muscle following transmural e lectrical stimulation (TES) of constrictor nerves or exposure to norep inephrine was depressed under acidic (pH 6.9) vs. control (pH 7.4) con ditions. Twenty mM K+-induced contractions were also inhibited by acid osis, however 40, 80, and 120 mM K+ contractions were unaffected. Rela xation responses to acetylcholine and electrical stimulation, in pheny lephrine contracted tissues, were unaffected by acidosis. Tissues cont racted with 20 mM K+ under control conditions, relaxed similar to 50% when exposed to an acidic environment. This relaxation was blocked by exposing the tissue to 80 mM K+. Acidic conditions inhibited basal ton e and [Ca2+](i) as well as normal increases in both intracellular free Ca2+ and tension upon exposure to 20 mM K+, while 80 mM K+-induced in creases in Ca2+ and tension were comparable under both neutral and aci dic conditions. Conclusion. Acidosis impairs trabecular smooth muscle contractility. This alteration is probably secondary to the interferen ce of [H+] with the intra and extracellular mechanisms that regulate h omeostasis of [Ca2+](i). Since acidosis is an early complication of is chemic priapism, we propose that the reduced contractility of trabecul ar smooth muscle may be a significant factor in the perpetuation of th e ischemic state.