Extracellular Ca2+ entry and mobilization of inositol trisphosphate-dependent Ca2+ stores modulate histamine and electrical field stimulation induced contractions of the guinea-pig prostate

This investigation aimed to examine the source of Ca2+ mobilization that leads to the contractile response to either exogenously added histamine (1 μM-1 mM) or electrical field stimulation (10 Hz, 0.5 ms, 60 V). Removal of extracellular Ca2+ by removal of Ca2+ from the bathing medium reduced histamine (1 mM) induced responses by 34% and responses induced by electrical field stimulation by 94%. Similarly, blockade of L-type Ca2+ channels by nifedipine (1 μM) reduced histamine (1 mM) induced responses by 43% and responses induced by electrical field stimulation by 77%. Application of cyclopiazonic acid (CPA) (10 μM) to inhibit Ca2+ reuptake to the sarcoplasmic reticulum enhanced both histamine-induced and electrical field stimulation induced responses to a small degree, while the addition of the inosotol triphosphate (IP3) receptor antagonist, 2-aminophenoxyethane borane (2-APB) (100 μM) inhibited histamine induced responses by 70% and electrical field stimulation induced responses by 57%. Ryanodine (1 μM) did not affect contractile responses to either histamine or electrical field stimulation, either in the absence or presence of 2-APB (100 μM). During both histamine and electrical field stimulation induced contractions, prostate smooth muscle generates IP3 receptor mediated Ca2+ release in conjunction with Ca2+ entry from the extracellular environment. Ryanodine receptors on the other hand, appear not to play a role in this physiological mechanism.

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