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This dissertation, Adrenomedullin in the Rat Testis: Its Production, Functions and Regulation in Sertoli Cells and Leydig Cells and Its Interaction With Endothelin-1 by Yuen-fan, Chan, 陳婉芬, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled ADRENOMEDULLIN IN THE RAT TESTIS: ITS PRODUCTION, FUNCTIONS AND REGULATION IN SERTOLI CELLS AND LEYDIG CELLS AND ITS INTERACTION WITH ENDOTHELIN-1 submitted by YUEN FAN CHAN for the degree of Master of Philosophy at the University of Hong Kong in August 2006 Since its discovery in 1993, adrenomedullin (AM) peptide and mRNA have been detected in the rat testis. AM and endothelin-1 (ET-1) are known to have opposite effects in many organs. In the rat testis, AM inhibits ET-1-induced peritubular myoid cell contraction. It is hypothesized that AM may exert autocrine/paracrine actions in the testis that are antagonistic to those of ET-1. The objectives of this project were to study the expressions of AM and its receptor components, their regulation by gonadotrophins and ET-1, and the effects of AM and its interaction with ET-1 in the rat Sertoli and Leydig cells. These cells were isolated from male Sprague-Dawley rats. Radioimmunoassay and enzyme immunoassay were used to quantify peptide and testosterone levels while mRNA levels were studied by RT-PCR. Both Sertoli and Leydig cells secreted AM peptide and expressed the mRNA of AM and its receptor components (CRLR, RAMP1, RAMP2 and RAMP3), with a higher CRLR and RAMP3 mRNA levels in Leydig cells but a higher RAMP1 mRNA level in Sertoli cells, indicating differential expressions of AM receptors in the rat testis. AM was found to stimulate testosterone production in the Leydig cell and inhibin production in the Sertoli cell in the basal states, but inhibit their gonadotrophin-stimulated secretions. Correlated with these, AM production in the Sertoli cells and Leydig cells was attenuated by both FSH and hCG respectively, suggesting that AM has functional roles in the testis including a hypothalamus- pituitary-gonad feedback loop. On the other hand, AM inhibited the production of ET-1, while AM production was enhanced by ET-1 in both the Sertoli and Leydig cells. The testosterone production triggered by ET-1 was suppressed by AM in the Leydig cell, in support of an AM/ET-1 antagonism. A local regulatory mechanism formed by AM and ET-1 that modulates the effects of gonadotrophins in the testis was suggested. In conclusion, AM is a novel paracrine factor that exerts autocrine/paracrine effects in the rat testis, at least partially, by interacting with ET-1. The AM/ET-1 regulatory mechanism suggested opens a new arena for research in male reproductive endocrinology. In the long term, the manipulation of the AM system may provide novel insight into the management of testicular disorders. DOI: 10.5353/th_b3744834 Subjects: AdrenomedullinSertoli cellsLeydig cellsEndothelinsGene expressionTestis - Molecular aspects

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