Behavioral and biochemical studies in rats following prenatal treatment with beta-adrenoceptor antagonists.
Increased motor activity and poor performance in the active avoidance test were observed in the offspring of rats treated with dl-propranolol or sotalol during pregnancy, but not with atenolol and d-propranolol. All substances were administered in drinking water from days 8-22 of gestation. A significant increase in the density of muscarinic acetylcholine receptors in the hippocampus was found for dl-propranolol and sotalol, at 35 and 20 days of age, respectively. Twenty-day-old pups born to dl-propranolol-treated rats exhibited a non-significant decrease in the number of beta-adrenoceptors in the frontal cortex. Assuming that all the beta-adrenoceptor antagonists tested had access to the developing fetal brain, the effect of dl-propranolol and sotalol on behavior could stem from central beta 2-adrenoceptor blockade. In view of the lack of behavioral changes after atenolol, a beta 1-selective adrenoceptor antagonist, it is suggested that the clinical use of beta 1-selective adrenoceptor antagonists during pregnancy might be safer for the fetus than beta 2-adrenoceptor antagonists.[1]References
- Behavioral and biochemical studies in rats following prenatal treatment with beta-adrenoceptor antagonists. Speiser, Z., Gordon, I., Rehavi, M., Gitter, S. Eur. J. Pharmacol. (1991) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg