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Relationship between gene expression of nitric oxide synthase and androgens in rat corpus cavernosum.
Chinese Medical Journal 2000 December
OBJECTIVE: To clarify the dependence of neural nitric oxide synthase mRNA (nNOSmRNA) and endothelial nitric oxide synthase mRNA (eNOSmRNA) on androgens (testosterone [T] and dihydrotestosterone [DHT]).
METHODS: 160 male Sprague Dawley (SD) rats were divided into Groups A (56 rats, 5 weeks old), B (50 rats, 10 weeks old) and C (54 rats, 58 weeks old). Groups A, B and C were all subdivided respectively into five Subgroups. Subgroup 1: intact controls; Subgroup 2: castrated; Subgroup 3: castrated with testosterone undecanoate 25 mg/kg.mon-1, intramuscular injection, Subgroup 4: castrated with testosterone undecanoate 50 mg/kg.mon-1, intramuscular injection and Subgroup 5: treated with finasteride 4.5 mg/kg.day-1, orally. Four and ten weeks after treatments described above, one half of the rats were killed. Serum samples were taken for measurements of T, free testosterone (FT) and DHT by radioimmunoassay. Penile samples were treated with liquid nitrogen and then stored at -80 degrees C. nNOSmRNA and eNOSmRNA were detected by semiquantitative reverse-transcription polymerase chain reaction (RT-PCR) and Dot blot.
RESULTS: There was no significant difference between Subgroup 1 and Subgroup 2 or Subgroup 5 in all Groups A, B and C. The expression of penile eNOSmRNA of Group A was significantly increased (4 weeks model) (P < 0.05) or increased (10 weeks model) (P > 0.05) in Subgroup 2 or 5 compared with those in Subgroup 1. There was no significant difference between Subgroup 1 and Subgroup 2 or Subgroup 5 of Group B in 4 weeks model (P > 0.05). There was an elevation when animals were castrated or treated with finasteride in the 10 weeks model. The expression of penile eNOSmRNA of Group C was significantly increased (10 weeks model) (P < 0.05) or increased (4 weeks model) in Subgroup 2 compared with those in Subgroup 1. The production of eNOSmRNA in Subgroup 5 was also increased (including 4- and 10-week models). When T was supplied for castration, the penile eNOSmRNA was decreased to some extent; the greater the dose of T given, the lower penile eNOSmRNA was observed.
CONCLUSIONS: The expression of eNOSmRNA in SD rat penile tissue increases while T or DHT diminishes. Sometimes androgens modulate penile eNOSmRNA in opposite directions. There is no correlation between the expression of nNOSmRNA and androgens (including T and DHT). Androgens give rise to penile erection probably not via the NOS pathway.
METHODS: 160 male Sprague Dawley (SD) rats were divided into Groups A (56 rats, 5 weeks old), B (50 rats, 10 weeks old) and C (54 rats, 58 weeks old). Groups A, B and C were all subdivided respectively into five Subgroups. Subgroup 1: intact controls; Subgroup 2: castrated; Subgroup 3: castrated with testosterone undecanoate 25 mg/kg.mon-1, intramuscular injection, Subgroup 4: castrated with testosterone undecanoate 50 mg/kg.mon-1, intramuscular injection and Subgroup 5: treated with finasteride 4.5 mg/kg.day-1, orally. Four and ten weeks after treatments described above, one half of the rats were killed. Serum samples were taken for measurements of T, free testosterone (FT) and DHT by radioimmunoassay. Penile samples were treated with liquid nitrogen and then stored at -80 degrees C. nNOSmRNA and eNOSmRNA were detected by semiquantitative reverse-transcription polymerase chain reaction (RT-PCR) and Dot blot.
RESULTS: There was no significant difference between Subgroup 1 and Subgroup 2 or Subgroup 5 in all Groups A, B and C. The expression of penile eNOSmRNA of Group A was significantly increased (4 weeks model) (P < 0.05) or increased (10 weeks model) (P > 0.05) in Subgroup 2 or 5 compared with those in Subgroup 1. There was no significant difference between Subgroup 1 and Subgroup 2 or Subgroup 5 of Group B in 4 weeks model (P > 0.05). There was an elevation when animals were castrated or treated with finasteride in the 10 weeks model. The expression of penile eNOSmRNA of Group C was significantly increased (10 weeks model) (P < 0.05) or increased (4 weeks model) in Subgroup 2 compared with those in Subgroup 1. The production of eNOSmRNA in Subgroup 5 was also increased (including 4- and 10-week models). When T was supplied for castration, the penile eNOSmRNA was decreased to some extent; the greater the dose of T given, the lower penile eNOSmRNA was observed.
CONCLUSIONS: The expression of eNOSmRNA in SD rat penile tissue increases while T or DHT diminishes. Sometimes androgens modulate penile eNOSmRNA in opposite directions. There is no correlation between the expression of nNOSmRNA and androgens (including T and DHT). Androgens give rise to penile erection probably not via the NOS pathway.
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