الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Varicocele is a pathologic enlargement of the pampiniform venous plexus within the spermatic cord. Varicocele is the most commonly identified and most common surgically correctable risk factor for male infertility. Not all males with varicocele present with infertility. Therefore, it is possible that different intrinsic susceptibilities exist among men with varicocele.
The pathophysiologic mechanism of varicocele associated infertility is not completely understood, the five following mechanisms are thought to contribute to the effect of varicocele on testicular function: hypoperfusion leading to hypoxia, heat stress, oxidative stress hormonal imbalances, and exogenous toxicants.
Varicocele is associated with stress pattern of semen analysis which entails reduced sperm count, motility and morphology but not semen volume.
Good sperm motility is a key component for normal male fertility and is currently the most reliable predictor of male infertility. Sperm motility proteins belong to diverse classes including ion channels, cytoskeletal proteins, glycolytic enzymes, and cell signaling proteins. Sperm fertility ability may be modulated by different communication systems.Among these peptide systems, opioids, tachykinins or the rennin-angiotensin system (RAS). The most studied function of rennin-angiotensin system is the regulation of blood pressure through electrolyte, and fluid homeostasis. In the classic RAS pathway, angiotensinogen is converted into angiotensin I (Ang I), catalyzed by rennin. Subsequently, angiotensin II (Ang II) is produced from angiotensin I by the angiotensin-converting enzyme. Angiotensin II is the most active peptide of the system. Angiotensin II is able to bind to two different receptors called angiotensin receptor type 1 (AT1R) and type 2 (AT2R), which are members of the G protein linked receptors.