title: Prorenin is elevated in polycystic ovary syndrome and may reflect hyperandrogenism.
abstract: OBJECTIVE
  To examine the null hypothesis that women with polycystic ovary syndrome (PCOS) produce similar levels of prorenin and other components of the ovarian-derived prorenin to angiotensin cascade (ODPAC) at baseline and after stimulation with clomiphene citrate (CC) or hMG when compared with normal age- and weight-matched ovulatory controls.
  
  
  METHODS
  Prospective controlled clinical trial.
  
  
  METHODS
  Infertility clinic in a university-based county hospital and a hospital-based private infertility practice.
  
  
  METHODS
  Twenty-eight infertile women aged 18 to 35 years. Thirteen patients were diagnosed with PCOS. Fifteen normal ovulatory patients who were matched for age and weight served as controls.
  
  
  METHODS
  Twenty patients were stimulated with CC and eight were stimulated with hMG.
  
  
  METHODS
  Serum E2, P, T, androstenedione (A), DHEAS, LH, FSH, and plasma prorenin, active renin, and angiotensin II (Ang II) were measured at baseline and during the preovulatory and midluteal phases of the stimulation cycles.
  
  
  RESULTS
  Baseline plasma prorenin in PCOS was higher than that of follicular phase controls. Plasma prorenin correlated significantly with peripheral androgen levels. Prorenin, active renin, and Ang II increased in response to gonadotropins with the largest increases occurring in control patients receiving CC. An association was seen between ovulation with CC and lower baseline levels of active renin.
  
  
  CONCLUSIONS
  The null hypothesis was rejected. Infertile women with PCOS have higher baseline prorenin levels when compared with age- and weight-matched ovulatory controls. There is a significant correlation between prorenin and the peripheral levels of androgens produced during ovarian stimulation. Baseline active renin levels may be predictive of ovulation with CC.
authors.affiliation: Division of Reproductive Endocrinology, University of Southern California School of Medicine, Los Angeles, USA.
authors.forename: R S
authors.initials: RS
authors.lastname: Morris
authors.forename: I L
authors.initials: IL
authors.lastname: Wong
authors.forename: I E
authors.initials: IE
authors.lastname: Hatch
authors.forename: E
authors.initials: E
authors.lastname: Gentschein
authors.forename: R J
authors.initials: RJ
authors.lastname: Paulson
authors.forename: R A
authors.initials: RA
authors.lastname: Lobo
mesh_terms: D000293:Adolescent; D000328:Adult; D000735:Androstenedione / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D002996:Clomiphene; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D004792:Enzyme Precursors / Q000097:blood*; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000097:blood*; D007247:Infertility, Female / Q000097:blood; D016555:Matched-Pair Analysis; D008596:Menotropins; D010062:Ovulation Induction; D011085:Polycystic Ovary Syndrome / Q000097:blood*; D011446:Prospective Studies; D012083:Renin / Q000097:blood*; D013739:Testosterone / Q000097:blood
chemical_list: D004792:Enzyme Precursors; D000804:Angiotensin II; D002996:Clomiphene; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D008596:Menotropins; D012083:Renin