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 intracellular fluorescent dye, FURA-2, and isometric tension recordings. Results. Contraction of corpus cavernosum smooth muscle following transmural electrical stimulation (TES) of constrictor nerves or exposure to norepinephrine was depressed under acidic (pH 6.9) vs. control (pH 7.4) conditions. Twenty mM K+-induced contractions were also inhibited by acidosis, however 40, 80, and 120 mM K+ contractions were unaffected. Relaxation responses to acetylcholine and electrical stimulation, in phenylephrine contracted tissues, were unaffected by acidosis. Tissues contracted 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 tone 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 increases in Ca2+ and tension were comparable under both neutral and acidic conditions. Conclusion. Acidosis impairs trabecular smooth muscle contractility. This alteration is probably secondary to the interference of [H+] with the intra and extracellular mechanisms that regulate homeostasis of [Ca2+](i). Since acidosis is an early complication of ischemic priapism, we propose that the reduced contractility of trabecular smooth muscle may be a significant factor in the perpetuation of the ischemic state.