ABSTRACT
Drugs could achieve uterine relaxation by several mechanisms. They have been subdivided into three strategies: functional antagonists, inhibitors of the production and/or release of spasmogens, and receptor antagonists. A functional antagonist will reduce the effect of a spasmogen by a biochemical mechanism opposite to that of the spasmogen, and, therefore, should attenuate the actions of a wide variety of spasmogens. There is substantial support for the idea that agonist-receptor interaction is linked to functional inhibition of contractions mainly via a G-protein-mediated stimulation of adenylyl cyclase. Drugs acting as inhibitors of the production and/or release of spasmogens could have a major impact in reducing uterine contractility if they inhibit an early stage in a biochemical cascade that results in the production of many myometrial spasmogens. Treatment of late pregnant/parturient rats with cyclo-oxygenase inhibitors results in very protracted deliveries, prolonged bleeding, and maternal and fetal/neonatal deaths.
