Ritopar

Ritodrine hydrochloride is a β2-adrenergic agonist. It works by stimulating the β2-adrenergic receptors in the muscle of the uterus, which relaxes the muscle and reduces both the strength and frequency of uterine contractions. At the cellular level, it raises cyclic adenosine monophosphate (cAMP) and increases cell-membrane cytokines that pull intracellular calcium into storage. Because contraction of the uterine muscle's contractile proteins depends on the availability of intracellular calcium, this drop in free calcium prevents the muscle from contracting, allowing the uterus to relax.

Ritodrine falls under pregnancy category B. Because there are no adequate, well-controlled studies of its effects before 20 weeks of gestation, it should not be given before the 20th week of pregnancy. Studies conducted from the 20th week onward have not shown an increased risk of fetal abnormalities. Even so, while clinical studies have not pointed to any lasting harm to the fetus, this possibility cannot be entirely ruled out, so the drug should be used only when clearly needed. Newborns are frequently reported to experience hypoglycemia and ileus, and low calcium levels and low blood pressure have been noted in infants whose mothers received other beta-mimetic agents during pregnancy. It should therefore be used with caution, and only when the expected benefit to the mother is judged to outweigh any possible risk to the infant.

An overdose of ritodrine can cause tachycardia (in both the mother and the fetus), palpitation, cardiac arrhythmia, hypotension, nervousness, tremor, nausea and vomiting.

If too many ritodrine tablets have been swallowed, the stomach should be emptied by gastric lavage or by inducing vomiting, and activated charcoal should be given afterwards. If the symptoms appear after parenteral use, ritodrine should be stopped. An appropriate β-blocking agent may be used as an antidote.

Keep Ritodrine Hydrochloride out of the reach of children. Store it in a cool, dry place, away from light.