https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35136 Wed 10 Nov 2021 15:04:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41393 Tue 02 Aug 2022 17:47:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18122 2+ 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.]]> Sat 24 Mar 2018 08:04:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38982 Mon 29 Jan 2024 17:51:56 AEDT ]]>