Voltage dependence of slow wave frequency in the guinea pig prostate

Spontaneous phasic contractions of the guinea pig prostate stroma result from the generation of slow waves that appear to primarily rely on spontaneous Ca(2+) release from the endoplasmic/sarcoplasmic reticulum and subsequent opening of Ca(2+) activated chloride channels. We investigated voltage dependent mechanisms in the regulation of slow wave frequency.

Changes in membrane potential were recorded using conventional intracellular recording techniques while simultaneously measuring the isometric tension of guinea pig prostate lobes. Fluorescence immunohistochemistry was done to determine the cellular composition of the prostate stroma.

Depolarization induced by high K(+) solution, K(+) free solution or outward current injection was associated with increased slow wave frequency. In contrast, hyperpolarization induced by the re-addition of K(+), adenosine triphosphate sensitive K(+) channel openers or inward current injection prevented slow wave generation. K(+) channel openers induced hyperpolarization and the cessation of slow waves was reversed by glibenclamide (10 μM). Nifedipine (1 to 10 μM) shortened the duration of slow waves and pacemaker potentials but often failed to prevent their generation and associated contractions. Subsequently Ni(2+) (100 μM) or mibefradil (1 μM) largely suppressed slow waves and abolished residual contractions. Immunohistochemistry revealed small interconnected smooth muscle bundles as well as vimentin positive interstitial cells but failed to show a network of Kit positive interstitial cells.

Prostate slow wave frequency is voltage dependent due to the significant contribution of L-type and T-type Ca(2+) channels. Prostate slow waves may arise from cooperation between spontaneous Ca(2+) release from internal stores and plasmalemmal voltage dependent Ca(2+) channels.