Role of mucosa in generating spontaneous activity in the guinea pig seminal vesicle.

KEY POINTS

The mucosa may have neuron-like functions as urinary bladder mucosa releases bioactive substances that modulate sensory nerve activity as well as detrusor muscle contractility. However, such mucosal function in other visceral organs remains to be established. The role of mucosa in generating spontaneous contractions in seminal vesicles (SVs), a paired organ in the male reproductive tract, was investigated. The intact mucosa is essential for the generation of spontaneous phasic contractions of SV smooth muscle arising from electrical slow waves and corresponding increases in intracellular Ca . These spontaneous events primarily depend on Ca handling by sarco-endoplasmic reticulum Ca stores. A population of mucosal cells developed spontaneous rises in intracellular Ca relying on sarco-endoplasmic reticulum Ca handling. The spontaneously active cells in the SV mucosa appear to drive spontaneous activity in smooth muscle either by sending depolarizing signals and/or by releasing humoral substances.

ABSTRACT

The role of the mucosa in generating the spontaneous activity of guinea-pig seminal vesicle (SV) was explored. Changes in contractility, membrane potential and intracellular Ca dynamics of SV smooth muscle cells (SMCs) were recorded using isometric tension recording, intracellular microelectrode recording and epi-fluorescence Ca imaging, respectively. Mucosa-intact but not mucosa-denuded SV preparations generated TTX- (1 μm) resistant spontaneous phasic contractions that were abolished by nifedipine (3 μm). Consistently, SMCs developed mucosa-dependent slow waves (SWs) that triggered action potentials and corresponding Ca flashes. Nifedipine (10 μm) abolished the action potentials and spontaneous contractions, while suppressing the SWs and Ca flashes. Both the residual SWs and spontaneous Ca transients were abolished by cyclopiazonic acid (CPA, 10 μm), a sarco-endoplasmic reticulum Ca -ATPase (SERCA) inhibitor. DIDS (300 μm) and niflumic acid (100 μm), blockers for Ca -activated Cl channels (CACCs), or low Cl solution also slowed or prevented the generation of SWs. In SV mucosal preparations detached from the muscle layer, a population of mucosal cells generated spontaneous Ca transients that were blocked by CPA but not nifedipine. These results suggested that spontaneous contractions and corresponding Ca flashes in SV SMCs arise from action potential generation due to the opening of L-type voltage-dependent Ca channels. Spontaneous Ca transients appear to primarily result from Ca release from sarco-endoplasmic reticulum Ca stores to activate CACCs to develop SWs. The mucosal cells firing spontaneous Ca transients may play a critical role in driving spontaneous activity of SV smooth muscle either by sending depolarizing signals or by releasing humoral substances.