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Abstract
Ritodrine hydrochloride is a β-mimetic amine which is used to inhibit premature labor.
While the mechanism of action of β-mimetic drugs is believed to be a function of its
action on the adenylate cyclase system, the drug may also act via other mechanisms.
We examined the effect of this drug on both contractile activity and prostanoid production
using an
preparation of a uterus from a 21-day pregnant rat. Two uterine segments were simultaneously
studied in separate incubation chambers.Ritodrine (2.0 mg/ml) was added to one tissue
chamber while the other tissue served as a control. Frequency and contractile force
were monitored polygraphically for 45 min.Incubation medium was then removed for analysis
of prostaglandin E2 (PGE2), PGF2α, 6-keto-PGF1α, and thromboxane B2 (TXB2) by radioimmunoassay. Ritodrine-treated uteri demonstrated a contractile force which
was 16.8% of that of the control, a significant decrease. Ritodrine-treated uteri
also produced less prostanoids. The greatest effect was on PGE production (27.3% of
the control, p <0.001). The effect of ritodrine on the other prostanoids was less
pronounced (PGF2α, 71%; 6-keto-PGF1α 84%; TXB2, 67% of the control). The presence of 0.2 mM dibutyryl cAMP in the incubation media
also suppressed contractile force; however, prostanoids were not reduced and in some
cases were elevated.It is concluded that one effect of ritodrine is a reduction in
prostanoid production, predominately PGE2 and this in part may play a role in the drug's efficacy. The reduction does not appear
to be mediated through the adenylate cyclase system.

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© 1984 Published by Elsevier Inc.