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. Author manuscript; available in PMC: 2016 Jul 1.
Published in final edited form as: Sex Med Rev. 2015 Jun 4;3(3):160–168. doi: 10.1002/smrj.56

Figure 1.

Figure 1

Schematic representation of the nitrergic mechanism underlying penile erection and contributing pathways which may offer targets for management of recurrent ischemic priapism. Decreased basal levels of PDE5 enzyme permits uncontrolled erection (priapism) because of the lack of the normal regulatory control mechanism involved in the return of the penis back to its flaccid state. Gray text represents current therapeutic approaches related to the nitrergic mechanism. White text represents potential pathways for future therapeutic approaches affecting the nitrergic mechanism. Circular arrows signify the pathway between penile erection states. Black arrows relate to the mechanism of penile erection. Gray arrows signify direct or indirect stimulation and gray T-shapes signify direct or indirect inhibition based on evidence suggesting associations of pathways in the setting of priapism. NO = nitric oxide, NOS = nitric oxide synthase, PDE5 = phosphodiesterase type 5, PDE5i = PDE5 inhibitor, TRT = testosterone replacement therapy