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This results in production of cAMP in the smooth muscle cell, activating PKA to minimize cytosolic Ca2+ focus. The prostanoids prostaglandin E2 (PGE2) and prostacyclin (PGI2) can additionally drive cAMP production through association with the EP and IP receptors on the smooth muscle mass cell, specifically. NANC coincides as shown in Figure 2sGC, PKG and NO are the same as received Figure 4. Interestingly, ET-1 signalling using the ETB receptor moderates smooth muscular tissue leisure. This is evident by injection of ET-1 right into the rat corpus cavernosum which causes both vasodilation and vasoconstriction [Ari et al., 1996] Furthermore, administration of an ETB agonist brings about leisure of the rat and computer mouse corpus cavernosum in vitro [Carneiro et al., 2008]
These results supply evidence that ET-1 drives smooth muscle contraction in the penis by boosting intracellular Ca2+ degrees and increasing Ca2+ sensitivity via PKC activation (Fig. 7). DAG, the various other product of PLC, activates protein kinase C (PKC) which can also drive smooth contraction [Hilgers and Webb, 2005] PKC phosphorylates the CPI-17 healthy protein, which in turn hinders MLCP (drives smooth muscular tissue relaxation) and hence enhances Ca2+ sensitization (Fig. 7) [Li et al., 1998; Nunes et al., 2010] CPI-17 is expressed in the human and rabbit corpus cavernosum, although to the best of our understanding, smooth muscle contraction in the penis mediated by PKC/CPI -17 signalling has yet to be confirmed [Jiang and Chitaley, 2012] Nonetheless, exposure of the rat corpus cavernosum to phorbol 12-myristate13-acetate (PMA) (PKC activator) potentiates phenylephrine-induced tightenings in vitro, while direct exposure to chelerythine chloride (PKC prevention) prevents it [Husain et al., 2004] This is additionally supported by the exposure of the rat corpus cavernosum to phenylephrine in vitro which causes increased degrees of PKC isozymes [Husain et al., 2004] Acetylcholine launched from cholinergic nerves binds to the muscarinic acetylcholine receptor (mAChR), which increases Ca2+ in the endothelial cell. Endogenous estrogen signalling additionally activates eNOS by promoting the PI3K/Akt pathway and upregulates expression of eNOS (see Fig. 5). Along with the NO-cGMP pathway, vasoactive intestinal tract peptide (VIP) in the NANC nerves might bind to its receptor (VIP-R) on the smooth muscle cell to promote soluble adenylyl cyclase (sAC).