Abstract
INTRODUCTION AND OBJECTIVES: Testosterone contributes signal pathway of penile erection and it is mainly secreted during sleep. However, there is no consensus that which level of the hormone axis will be mainly affected to sleep deprivation (SD). So, we investigated whether 1) SD could alter the hormonal axis or not, 2) which level of the axis could be the major target of SD and 3) subsequently whether SD could decrease erectile function or not. METHODS: 32 Wistar rats (16 weeks old) were divided into 2 groups. Using automated sleep deprivation system (Pinnacle technology inc. USA), sleep deprivation for 48~56 hours was done in experimental group. Then, cavernous nerve on posterolateral aspect of the prostate was stimulated with electrode. Intracavernosal pressure was checked during carotid arterial pressure monitoring. Blood sample was collected by puncturing of left cardiac ventricle. After sacrifice of a rat, brain tissue was extracted for measuring Kisspeptin mRNA, and fluorescence stains were done with testis (P450scc stain, stAR stain) and penile tissue (nNOS, eNOS). RESULTS: Kisspeptin mRNA, gonadotropin releasing hormone, follicular stimulating hormone were not different between two groups. Luteinizing hormone and testosterone were significantly different between two groups (a_image). Steroidogenesis in the leydig cell was more prominent in control group than in experimental group. Positive area of cavernous nerve with nNOS staining and that of penile smooth muscle with eNOS staining were decreased in SD group. Intracavernosal pressure also decreased in SD group (b_image). CONCLUSIONS: Acute SD may mainly exert influence on luteinizing hormone secretion in anterior hypophysis. Subsequently, the result decreases the steroidogenesis in leydig cell, resultantly decline of testosterone would develop. These chain-reactions of the hormone axis would be a factor of lowering the erectile function. Source of Funding: None
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