Myometrial relaxants

If labour begins prematurely, before 33 weeks gestation, myometrial relax-ants (tocolytic agents) can delay it for 48 hours. Beta-2-agonists, such as ritodrine hydrochloride, are given for up to 48 hours to elicit relaxation. Longer treatment is not recommended, because of risk of adverse effects on the mother. Nifedipine and the oxytocin receptor antagonist atosiban are also used to reduce premature uterine contractile activity. 

Clenbuterol p2-Adrenoceptor Bronchodilation myometrial relaxation (cows)... 

Uterine relaxation is mediated in part through inhibition of MLCK. This inhibition results from the phosphorylation of MLCK that follows the stimulation of myometrial (3-adrenoceptors relaxation involves the activity of a cyclic adenosine monophosphate (cAMP) mediated protein kinase, accumulation of Ca++ in the sarcoplasmic reticulum, and a decrease in cytoplasmic Ca. Other circulating substances that favor quiescence of uterine smooth muscle include progesterone, which increases throughout pregnancy, and possibly prostacyclin. Progesterone s action probably involves hyperpolarization of the muscle cell membrane, reduction of impulse conduction in muscle cells, and increased calcium binding to the sarcoplasmic reticulum. 

Q9 Myometrial contractile activity is modified by both endocrine and autonomic factors. The increase in oestrogens during pregnancy gradually increases both the excitability of uterine smooth muscle and its sensitivity to agonists, particularly oxytocin. The uterus receives sympathetic innervation, which exerts excitatory effects via alpha-1-receptors (a i-receptors). Uterine smooth muscle also possesses beta-2-receptors (/d2-recept°rs)> which mediate relaxation. 

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