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Furthermore, the TP receptor can turn on RhoGEF, which consequently activates RhoA [Feletou, 2010] Hence, TXA2 through its receptor may drive smooth contraction in the penis by boosting cytosolic Ca2+ and promoting the RhoA/Rho-kinase path (Fig. 7). Undoubtedly, TP receptors are identified as contractile factors of human penile arteries and trabecular smooth muscular tissue in vitro [Angulo et al., 2002] Also, therapy of rat spacious arteries with the TXA2 analogue U46619 resulted in enhanced Ca2+ focus and contraction artificial insemination [Grann et al., 2016] The writers additionally found that treatment of the Rho-kinase preventions Y27632 and glycyl-H1152P dose-dependently undermined U46619-induced tightening, providing additional evidence that TXA2 moderates contraction using activating the RhoA/Rho-kinase path.
Subsequently, cGMP activates protein kinase G (PKG) which decreases Ca2+ focus via numerous mechanisms [Ghalayini, 2004; Krassioukov and Elliott, 2017] This includes phosphorylation of K+ networks, which results in an efflux of K+ and subsequent hyperpolarization of smooth muscle mass cells within the penis [Archer, 2002] Hyperpolarization shuts voltage-dependent Ca2+ networks, consequently reducing the influx of Ca2+ into smooth muscular tissue cells [Andersson and Wagner, 1995]