Ritodrine: effects

Mechamism of Action

Ritodrine is a selective beta-2 receptor agonist that developed specifically for use as a uterine relaxant. Ritodrine suppress premature uterine contractions through their effects on increase in intracellular cyclic adenosine monophosphate (cAMP) and relaxes uterine smooth muscles.

Intended Use

Uterine Relaxant

Side Effects

Cardiac Effects (Tachycardia)

Tachycardia is a common adverse effect of systemically administered receptor agonists. Stimulation of heart rate occurs primarily via beta-1 receptors. It is uncertain to what extent the increase in heart rate also is due to activation of cardiac beta-2 receptors or to reflex effects that stem from beta-2 receptor–mediated peripheral vasodilation. However, during a severe asthma attack, heart rate actually may decrease during therapy with a beta agonist, presumably because of improvement in pulmonary function with consequent reduction in endogenous cardiac sympathetic stimulation. In patients without cardiac disease, agonists rarely cause significant arrhythmias or myocardial ischemia; however, patients with underlying coronary artery disease or preexisting arrhythmias are at greater risk. The risk of adverse cardiovascular effects also is increased in patients who are receiving MAO inhibitors. In general, at least 2 weeks should elapse between the use of MAO inhibitors and administration of beta-2 receptor agonists or other sympathomimetics. Tremor is also notable along with other beta-1 effects with ritadrine

Pulmonary Edema

Pulmonary edema from ritodrine in obsetric anesthesia has been well noted, but its mechanism is not completely known, putative theories include increase in ADH that aggravate the already expanded intravascular volume of pregnancy. Instances of tocolytic related pulmonary edema with normal pulmonary occlusion pressures, however, argue against this mechanism. It is also possible that fluid infusions used to manage the systemic vasodilation of drug therapy with beta-agonists present a volume overload when vasoconstriction occurs after discontinuation of tocolytic therapy. A pulmonary capillary leak phenomenon may also participate in pathogenic mechanisms. Although exact mechanisms remain elusive, pulmonary edema may occur from varying degrees of heart failure, pulmonary vasoconstriction, capillary leak syndrome, intravascular volume overload, and reduced serum oncotic pressure.

Theoretical Concerns re: long term beta-2-selective receptor agonists

Long use of beta-2-selective receptor agonists have been known to cause death or near-death from asthma possibly through downregulation of receptors in some tissues and decreased pharmacological responses and through increased bronchial hyperreactivity and deterioration in disease control, but this concept is not well know with the use of ritodrine as it is only administered on a temporary basis.

Gluconeogenesis

Ritodrine may also increase the concentrations of glucose through gluconeogenesis, this has to be noted in diabetic patients, as higher doses of insulin may be required.

Effects on Potassium (Hypokalemia)

Decrease in the concentration of potassium is also well known. The decrease in potassium concentration may be especially important in patients with cardiac disease, particularly those taking digoxin and diuretics.