The polyamines have been postulated to be essential in most processes associated with both hypertrophy and hyperplasia.
The effects of estrogen on uterine contractility vary with animal species, and most reports have shown that in vitro contractility of rat uterus is decreased after estrogen treatment, but estrogen increases polyamine contents in castrated rat uterus.
This study was carried out to investigate whether the regulation of polyamine metabolism may be instrumental in the contractile response of castrated nonpregnant uterus of female SD rats to electrical field stimulation (40 V, 100 μsec : EFS). Estradiol (E2) increased uterine contents of putrescine (PT), spermidine (SPD), and spermine (SPM). These E2 effects were inhibited by tamoxifen or DFMO, but E2-incuced increase of uterine SPM content was enhanced by aminoguanidine.
E2 decreased the amplitude of force developed in the rhythmic spontaneous contraction of rat uterus, but it exaggerated the increase of uterine contraction force in response to EFS.
The E2-dependent exaggeration was inhibited by tamoxifen, DFMO, or indomethacin, but was significantly enhanced by aminoguanidine.
The synergism between E2 and aminoguanidine on uterine contractility was little affected by indomethacin.
These results suggest that E2-dependent increase of uterine contractility may be ascribed partly to increase of uterus polyamines.
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