Disease relevance of ritodrine

• Treatment of preterm labor with the beta-adrenergic agonist ritodrine [1].
• Pulmonary edema after ritodrine therapy in a patient with preeclampsia [2].
• Sinus bradycardia following ritodrine withdrawal [3].
• Fetal death associated with severe ritodrine induced ketoacidosis [4].
• We conclude that ritodrine and terbutaline induce profound hypokalemia by stimulating cellular potassium uptake and both drugs cause significant renal sodium and fluid retention and cardiac arrhythmias [5].

High impact information on ritodrine

• Zn2+ also inhibited lipolysis stimulated by the beta-adrenergic agent ritodrine in the absence of glucose [6].
• More importantly, lipolysis stimulated submaximally with ritodrine (10(-7) M) or glucagon (10(-9) M) was inhibited by H2O2 in a manner similar to insulin, although slight differences in time course were noted [7].
• The beta 2 activity of ritodrine produces the relaxation of smooth muscles and is believed to act directly on the beta 2-receptors of the myometrium [8].
• Studies on animal models indicate that the sulfate conjugate is a major urinary metabolite of ritodrine [8].
• Ritodrine pharmacokinetics [9].

Chemical compound and disease context of ritodrine

• The effects of ritodrine and terbutaline on potassium homeostasis, renal function, and cardiac rhythm were assessed in women treated with these drugs for preterm labor [5].
• Changes in acid-base homeostasis, plasma aldosterone, or renal potassium excretion did not contribute to ritodrine-or terbutaline-induced hypokalemia [5].
• A 19-yr-old woman developed adult respiratory distress syndrome (ARDS) in the postnatal period after treatment with dexamethasone and ritodrine for premature labor [10].
• Ephedrine remains the vasopressor of choice for treatment of hypotension during ritodrine infusion and epidural anesthesia [11].
• One of these agents, ritodrine hydrochloride, is the only Federal Drug Administration (FDA) approved drug for the treatment of preterm labor [12].

Biological context of ritodrine

• Moreover, 1 microM ritodrine, which is known to relax uterine muscle contraction, attenuated oxytocin-induced MAP kinase activity and phosphorylation [13].
• To determine the effects of fetal beta-2 agonist exposure on fetal hepatic glycogen metabolism, we infused ritodrine at a rate of 1.3 +/- 0.4 microgram/kg/min (mean +/- SD) for 24 h into six chronically catheterized twin fetal lambs starting between 128 and 134 days gestation [14].
• Infusion of ritodrine increased maternal heart rate 18 +/- 1% (P less than .0001), decreased maternal mean arterial pressure (MMAP) 4 +/- 1% (P less than .01), and decreased UBFV 5 +/- 1% (P less than .001) [15].
• At 120 min ritodrine had increased maternal cardiac output 45 +/- 6% above baseline (P = 0.0001) in the ritodrine-lidocaine group and 39 +/- 6% above baseline (P = 0.0001) in the ritodrine-NS group [16].
• To assess the effect of septal hypertrophy on cardiac function we obtained M-mode echocardiograms on day 1 of life in 41 infants exposed to ritodrine and 22 control infants matched for gestational age [17].

Anatomical context of ritodrine

• The amniotic fluid was also analyzed for conjugated metabolites of ritodrine [18].
• Samples were collected from the fetal femoral artery, umbilical vein, maternal femoral artery, uterine vein, fetal trachea and the amniotic activity for ritodrine quantitation [18].
• Plasma levels of ritodrine (20.0 +/- 2.7 ng/ml) were within the range of those reported in human fetuses exposed to ritodrine tocolysis [19].
• 2 In the longitudinal muscle cells of the 22nd day of gestation, ritodrine (greater than 10(-8) M) hyperpolarized the membrane, reduced the membrane resistance and suppressed the amplitude of contraction [20].
• Ritodrine infusion was associated with statistically significant metabolic and pulmonary effects in comparison with twin controls [21].

Associations of ritodrine with other chemical compounds

• Potentiometry reveals a very sensitive CE detection mode, with sub-micromolar detection limits for amines and the randomly chosen drugs quinine, clozapine, cocaine, heroine, noscapine, papaverine, and ritodrine [22].
• To study the effects of beta-2 agonist on metabolic regulation in fetal lamb lung, ritodrine hydrochloride, a preferential beta-2 agonist, was infused i.v. at a rate of 1.3 +/- 0.4 micrograms/kg/min (mean +/- S.D.) for 24 hr into six twin chronically catheterized fetal lambs starting between 0.86 and 0.91 gestation [23].
• Our data suggest that in infants weighing less than 1,000 g, control of labor with ritodrine for a minimum of 24 hours and administration of betamethasone can reduce significantly not only the incidence of respiratory distress syndrome but also mortality and morbidity [24].
• Evidence that an atypical beta-adrenoceptor mediates the inhibition of spontaneous rhythmical contractions of rabbit isolated jejunum induced by ritodrine and salbutamol [25].
• The agonists used were isoprenaline, oxyfedrine (atria only) and (except in brown adipocytes) ritodrine, which was a partial agonist in white adipocytes, atria and vas deferens [26].

Gene context of ritodrine

• Ritodrine, which is known to relax uterine muscle contraction, attenuated ET-1-induced MAP kinase activity [27].
• In this study, we aimed to investigate the activities of ritodrine sulfation by SULT1A1, which is expressed predominantly in the liver, and SULT1A3, which is expressed predominantly in the intestine, as well as the inhibitory effects of beverages on their activities [28].
• Inhibitory effects of various beverages on ritodrine sulfation by recombinant human sulfotransferase isoforms SULT1A1 and SULT1A3 [28].
• 2. to compare these effects with those of the beta-2 adrenoreceptor agonist, ritodrine [29].
• CONCLUSIONS: The beta-3 adrenoreceptor agonist BRL 37344 induced relaxation of human myometrial contractions with similar potency to that of the most commonly used tocolytic agent ritodrine [29].

Analytical, diagnostic and therapeutic context of ritodrine

• Plasma and urine ritodrine (free and conjugated) were determined with HPLC by electrochemical detection [9].
• During Holter monitoring, 3 of 14 women treated with ritodrine or terbutaline developed symptomatic cardiac arrhythmias at the lowest plasma potassium while no women treated with saline and morphine (N = 12) developed cardiac arrhythmias (P = 0.14) [5].
• CONCLUSIONS: Our data indicate that maternal MgSO4 treatment, in contrast to antenatal ritodrine, is associated with lowered cerebral perfusion in preterm infants on the first day of life [30].
• The effect of vasopressor agents upon uterine artery blood flow velocity in the gravid guinea pig subjected to ritodrine infusion [15].
• Does ritodrine worsen maternal hypotension during epidural anesthesia in gravid ewes [16]?

References