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These results give evidence that ET-1 drives smooth contraction in the penis by enhancing intracellular Ca2+ levels and boosting Ca2+ sensitivity via PKC activation (Fig. 7). DAG, the other product of PLC, activates healthy protein kinase C (PKC) which can additionally drive smooth muscle contraction [Hilgers and Webb, 2005] PKC phosphorylates the CPI-17 healthy protein, which subsequently prevents MLCP (drives smooth muscle leisure) and thus enhances Ca2+ sensitization (Fig. 7) [Li et al., 1998; Nunes et al., 2010] CPI-17 is revealed in the human and rabbit corpus cavernosum, although to the very best of our knowledge, smooth muscle contraction in the penis mediated by PKC/CPI -17 signalling has yet to be proven [Jiang and Chitaley, 2012] Nevertheless, exposure of the rat corpus cavernosum to phorbol 12-myristate13-acetate (PMA) (PKC activator) potentiates phenylephrine-induced contractions in vitro, while exposure to chelerythine chloride (PKC inhibitor) prevents it [Husain et al., 2004] This is also supported by the direct exposure of the rat corpus cavernosum to phenylephrine in vitro which results in increased levels of PKC isozymes [Husain et al., 2004] This is sustained by ET-1 therapy of the rabbit corpus cavernosum which leads to accumulation of inositol phosphates artificial insemination, suggesting that ET-1 likewise triggers PLC in this tissue [Holmquist et al., 1992] Likewise, endothelin-induced contractions of the bunny and human corpus cavernosum are lowered in Ca2+- cost-free remedy, or after therapy with nimodipoine (Ca2+ network blocker) [Holmquist et al., 1990] This shows that ET-1 signalling partially depends on Ca2+ influx to drive smooth muscle contraction. Additionally, therapy of the bunny corpus cavernosum with H7 (PKC inhibitor) lowers ET-1-mediated contraction artificial insemination and abolishes it in Ca2+- totally free service [Holmquist et al., 1990]