https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47519 Wed 24 Jan 2024 14:11:41 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27510 Wed 11 Apr 2018 11:48:28 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53689 Wed 10 Jan 2024 10:35:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45587 2+) release-refill cycle of Ca²⁺ stores. This occurs through opening of inositol 1,4,5-trisphosphate receptor (IP₃R)- and/or ryanodine receptor (RyR)-operated Ca²⁺ release channels in the sarcoplasmic/endoplasmic (SR/ER) reticulum and refilling by the SR/ER reticulum Ca²⁺ATPase (SERCA). Released Ca²⁺ from stores near the plasma membrane diffuse through the cytosol to open Ca2²⁺-activated chloride (Cl⁻) channels, this generating inward current through an efflux of Cl⁻. The resultant depolarisation leads to the opening of voltage-dependent Ca²⁺ channels and possibly increased production of IP3, which through Ca²⁺-induced Ca²⁺ release (CICR) of IP₃Rs and/or RyRs and IP₃R-mediated Ca²⁺ release provide a means by which store oscillators entrain their activity. Intercellular entrainment normally involves current flow through gap junctions that interconnect mural cells and in many cases this is aided by additional connectivity through the endothelium. Once entrainment has occurred the substantial Ca²⁺ entry that results from the near-synchronous depolarisations leads to rhythmical contractions of the mural cells, this often leading to vessel constriction. The basis for venous/venular vasomotion has yet to be fully delineated but could improve both venous drainage and capillary/venular absorption of blood plasma-associated fluids.]]> Wed 02 Nov 2022 09:13:14 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34620 Thu 04 Apr 2019 14:26:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:9515 Sat 24 Mar 2018 08:35:35 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1408 Sat 24 Mar 2018 08:28:15 AEDT ]]> https://ogma.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 ]]>