Effects of 17beta-estradiol on rat urinary bladder: gender differences in anoxia-glucopenia and reperfusion damage.
OBJECTIVE
To study the effect of 17beta-estradiol (E(2)) as a neuroprotective agent in male and female rat urinary bladders subjected to anoxia-glucopenia and reperfusion (A/G-R) damage.


METHODS
Rat urinary bladders were exposed to 1 hour of A-G and 2 hours of reperfusion (R). Intrinsic nerves underwent electrical field stimulation. The effect of E(2) on the contractile response and its recovery in R phase, was monitored by adding it to the bath medium, at different concentrations, 60 min before A-G, during the A-G and the first 30 min of R. Furthermore, on both genders, in vivo treatments with E(2), testosterone, IC1 182,780 and anastrozole were performed.


RESULTS
After A-G the recovery of the nerve function in female bladders were significantly higher than in male. E(2) given both in vivo (increased of E(2) plasma levels were monitored) and in vitro, resulted to be neuroprotective in male bladder subjected to A-G/R damage. When rats were treated with anastrozole, a lower recovery of nerve responses both in male and female bladders was observed. Finally, treatments with E2 receptor antagonist ICI 182,780 increased E(2) plasma levels and showed to abolished E(2) neuroprotection, thus suggesting that E2 promotes neuronal survival likely through a rapid estrogen receptor mediated response.


CONCLUSIONS
Male rat urinary bladder serves are more susceptible to A-G/R damage than female. E(2) exhibits neuroprotective properties and could be a lead for novel agents capable to protect the urinary bladder from ischaemia/reperfusion damage associated with urinary bladder disorders.
Valeri
Aurora
A
Department of Neuroscience, Siena University, Siena, Italy.
Ceccarelli
Ilaria
I
Fiorenzani
Paolo
P
Aloisi
Anna Maria
AM
Sgaragli
Giampietro
G
Pessina
Federica
F
D000077384:Anastrozole; D000818:Animals; D047072:Aromatase Inhibitors / Q000494:pharmacology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D004958:Estradiol / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000097:blood / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D005260:Female; D000077267:Fulvestrant; D005947:Glucose / Q000172:deficiency*; D000860:Hypoxia / Q000188:drug therapy* / Q000503:physiopathology; D066298:In Vitro Techniques; D007279:Injections, Subcutaneous; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D009570:Nitriles / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000503:physiopathology; D012737:Sex Factors; D013739:Testosterone / Q000494:pharmacology; D013997:Time Factors; D014230:Triazoles / Q000494:pharmacology; D001743:Urinary Bladder / Q000187:drug effects* / Q000294:innervation / Q000503:physiopathology; D001745:Urinary Bladder Diseases / Q000188:drug therapy* / Q000503:physiopathology
D047072:Aromatase Inhibitors; D004965:Estrogen Antagonists; D018696:Neuroprotective Agents; D009570:Nitriles; D014230:Triazoles; D000077267:Fulvestrant; D000077384:Anastrozole; D013739:Testosterone; D004958:Estradiol; D005947:Glucose