Characteristics of spontaneous activity in the bladder trigone

During bladder filling, the trigone contracts help keep the ureteral orifices open and the bladder neck shut. The trigone generates spontaneous activity as well as responding to neuromuscular transmitters, but the relationship between these phenomena are unclear.

To characterise the cellular mechanisms that regulate and modify spontaneous activity in trigone smooth muscle.

Muscle strips from the superficial trigone of male guinea-pigs were used for tension experiments and immunofluorescent studies.

In isolated trigonal cells, intracellular Ca(2+) was measured by epifluorescence microscopy using the fluorescent Ca(2+) indicator Fura-2.

Spontaneous intracellular Ca(2+) transients and contractions were observed in trigonal single cells and strips and were significantly higher compared to the bladder dome. Ca-free superfusate and verapamil terminated spontaneity. T-type Ca(2+) channel block with NiCl(2) depressed slightly Ca(2+) transients but not spontaneous contractions. Neither the BK(Ca) channel blocker iberiotoxin nor the SK(Ca) channel blocker apamin had any effect on single cell activity. By contrast, the Cl(-) channel blocker niflumic acid attenuated significantly both Ca(2+) transients and muscle contractions. Agonist stimulation (carbachol, phenylephrine) up-regulated activity. Gap junction labelling (Cx43) was approximately 5 times denser in the trigone than in detrusor smooth muscle. The gap junction blocker 18-beta-glycyrrhetinic acid modulated spontaneous contractions in the trigone but not in the bladder dome.

Trigone myocytes employ membrane L-type-Ca(2+) channels and Cl(-) channels to generate spontaneous activity. Intercellular electrical coupling ensures its propagation and, thus, sustains contraction of the whole trigone.