Bisphenol A attenuates phenylbiguanide-induced cardio-respiratory reflexes in anaesthetized rats
► Effect of bisphenol A (BPA) on phenylbiguanide (PBG)-induced reflexes was examined. ► Chronic ingestion of BPA (2μg/kg) attenuated PBG-induced reflexes. ► Acute intravenous injection of BPA also attenuated PBG-reflex response. ► Attenuation of PBG-reflex by BPA was seen with decreased vagal affere...
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Published in | Neuroscience letters Vol. 530; no. 1; pp. 69 - 74 |
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Abstract | ► Effect of bisphenol A (BPA) on phenylbiguanide (PBG)-induced reflexes was examined. ► Chronic ingestion of BPA (2μg/kg) attenuated PBG-induced reflexes. ► Acute intravenous injection of BPA also attenuated PBG-reflex response. ► Attenuation of PBG-reflex by BPA was seen with decreased vagal afferent activity. ► BPA by attenuating the visceral reflexes may produce cardio-respiratory changes.
Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex apnoea induced by the vagal C fibre stimulation. Therefore, the present study was undertaken to examine the effects of chronic and acute exposure to BPA on cardio-respiratory reflexes elicited by phenylbiguanide (PBG). Acute and chronic experiments were performed on adult female rats. In chronic experiments, the animals were ingested with pellets containing BPA (2μg/kg body weight) or without BPA (time-matched control) for 30 days. Subsequently, the animals were anaesthetized and prepared for recording blood pressure, ECG and respiratory excursions. PBG was injected through jugular vein to evoke reflexes in these animals. In acute experiments, the PBG reflexes were obtained before and after injecting BPA/ethanol. Also vagal afferent activity was recorded in some rats. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. The maximal changes were around 50–65%. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. Acute exposure of animals to BPA (35mg/kg body weight) for 30min also attenuated the PBG-induced responses significantly. The attenuation of the PBG reflex responses by BPA in acute experiments was associated with decreased vagal afferent activity. The present results indicate that BPA attenuates the protective cardio-respiratory reflexes due to decreased vagal afferent activity. |
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AbstractList | Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex apnoea induced by the vagal C fibre stimulation. Therefore, the present study was undertaken to examine the effects of chronic and acute exposure to BPA on cardio-respiratory reflexes elicited by phenylbiguanide (PBG). Acute and chronic experiments were performed on adult female rats. In chronic experiments, the animals were ingested with pellets containing BPA (2 mu g/kg body weight) or without BPA (time-matched control) for 30 days. Subsequently, the animals were anaesthetized and prepared for recording blood pressure, ECG and respiratory excursions. PBG was injected through jugular vein to evoke reflexes in these animals. In acute experiments, the PBG reflexes were obtained before and after injecting BPA/ethanol. Also vagal afferent activity was recorded in some rats. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. The maximal changes were around 50a65%. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. Acute exposure of animals to BPA (35 mg/kg body weight) for 30 min also attenuated the PBG-induced responses significantly. The attenuation of the PBG reflex responses by BPA in acute experiments was associated with decreased vagal afferent activity. The present results indicate that BPA attenuates the protective cardio-respiratory reflexes due to decreased vagal afferent activity. Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex apnoea induced by the vagal C fibre stimulation. Therefore, the present study was undertaken to examine the effects of chronic and acute exposure to BPA on cardio-respiratory reflexes elicited by phenylbiguanide (PBG). Acute and chronic experiments were performed on adult female rats. In chronic experiments, the animals were ingested with pellets containing BPA (2 μg/kg body weight) or without BPA (time-matched control) for 30 days. Subsequently, the animals were anaesthetized and prepared for recording blood pressure, ECG and respiratory excursions. PBG was injected through jugular vein to evoke reflexes in these animals. In acute experiments, the PBG reflexes were obtained before and after injecting BPA/ethanol. Also vagal afferent activity was recorded in some rats. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. The maximal changes were around 50-65%. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. Acute exposure of animals to BPA (35 mg/kg body weight) for 30 min also attenuated the PBG-induced responses significantly. The attenuation of the PBG reflex responses by BPA in acute experiments was associated with decreased vagal afferent activity. The present results indicate that BPA attenuates the protective cardio-respiratory reflexes due to decreased vagal afferent activity. ► Effect of bisphenol A (BPA) on phenylbiguanide (PBG)-induced reflexes was examined. ► Chronic ingestion of BPA (2μg/kg) attenuated PBG-induced reflexes. ► Acute intravenous injection of BPA also attenuated PBG-reflex response. ► Attenuation of PBG-reflex by BPA was seen with decreased vagal afferent activity. ► BPA by attenuating the visceral reflexes may produce cardio-respiratory changes. Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex apnoea induced by the vagal C fibre stimulation. Therefore, the present study was undertaken to examine the effects of chronic and acute exposure to BPA on cardio-respiratory reflexes elicited by phenylbiguanide (PBG). Acute and chronic experiments were performed on adult female rats. In chronic experiments, the animals were ingested with pellets containing BPA (2μg/kg body weight) or without BPA (time-matched control) for 30 days. Subsequently, the animals were anaesthetized and prepared for recording blood pressure, ECG and respiratory excursions. PBG was injected through jugular vein to evoke reflexes in these animals. In acute experiments, the PBG reflexes were obtained before and after injecting BPA/ethanol. Also vagal afferent activity was recorded in some rats. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. The maximal changes were around 50–65%. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. Acute exposure of animals to BPA (35mg/kg body weight) for 30min also attenuated the PBG-induced responses significantly. The attenuation of the PBG reflex responses by BPA in acute experiments was associated with decreased vagal afferent activity. The present results indicate that BPA attenuates the protective cardio-respiratory reflexes due to decreased vagal afferent activity. |
Author | Pant, Jayanti Pant, Mahendra K. Deshpande, Shripad B. |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23041044$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_2903_j_efsa_2015_3978 crossref_primary_10_2903_j_efsa_2023_6857 crossref_primary_10_3390_toxics8020034 crossref_primary_10_3389_fphys_2021_638506 crossref_primary_10_1016_j_neuroscience_2015_01_010 crossref_primary_10_1515_jbcpp_2017_0068 crossref_primary_10_4161_endo_26490 |
Cites_doi | 10.1289/ehp.10753 10.1111/j.1476-5381.2010.00687.x 10.1210/en.2004-1018 10.1111/j.1469-7793.1999.00537.x 10.1016/S0079-6123(08)63010-1 10.1289/ehp.5993 10.1542/peds.113.5.e429 10.1016/j.neuro.2006.10.001 10.1371/journal.pone.0008673 10.1210/en.2011-1772 10.1152/physrev.1991.71.3.617 10.1289/ehp.95103608 10.1155/2012/481641 10.1016/S0041-0101(99)00112-9 10.1007/s00204-001-0319-1 10.1016/j.neulet.2012.04.044 10.1111/j.1748-1716.2008.01953.x 10.1152/physrev.1973.53.1.159 10.1016/j.toxicon.2010.11.010 10.1001/jama.300.11.1303 10.1002/jat.1647 10.1093/toxsci/68.2.339 10.4315/0362-028X-66.8.1444 10.1016/S0300-483X(03)00056-8 10.1111/j.1748-1716.2010.02105.x 10.1038/sj.jea.7500174 |
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Keywords | J-reflex Pulmonary C reflex Visceral reflexes Vagal afferent activity Toxic effects of BPA |
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Snippet | ► Effect of bisphenol A (BPA) on phenylbiguanide (PBG)-induced reflexes was examined. ► Chronic ingestion of BPA (2μg/kg) attenuated PBG-induced reflexes. ►... Bisphenol A (BPA), a toxic chemical released from plastics, produces respiratory arrest and hypotension after a latency. The latency was similar to the reflex... |
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SubjectTerms | Air Pollutants, Occupational - toxicity Analgesics - pharmacology Anesthesia Animals Apnea Benzhydryl Compounds - toxicity Biguanides - pharmacology Bisphenol A Blood pressure Blood Pressure - drug effects Body weight Bradycardia Central Nervous System Depressants - pharmacology Drug Interactions EKG Electrocardiography - drug effects Ethanol Ethanol - pharmacology Female Heart rate Heart Rate - drug effects Hypotension J-reflex Jugular vein Nervous system Neurons, Afferent - drug effects Phenols - toxicity phenylbiguanide Plasticity Plastics - toxicity Pulmonary C reflex Rats Rats, Inbred Strains Reflex - drug effects Reflexes Respiration Respiratory Mechanics - drug effects Sensory neurons Sleep disorders Toxic effects of BPA Vagal afferent activity Vagus nerve Vagus Nerve - drug effects Visceral reflexes |
Title | Bisphenol A attenuates phenylbiguanide-induced cardio-respiratory reflexes in anaesthetized rats |
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