Endothelins and rat carotid body: autoradiographic and functional pharmacological studies
| Autor: | S.M. Bond, C.G. Marr, V.J. Cobb, Daniel S. McQueen, Michael R. Dashwood, K M Spyer |
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| Rok vydání: | 1995 |
| Předmět: |
Endothelin Receptor Antagonists
Male medicine.hormone medicine.medical_specialty Indoles Physiology Biology Iodine Radioisotopes Endothelins Internal medicine Hyperventilation medicine Animals Rats Wistar Respiratory system Hypoxia Carotid Body Cyanides General Neuroscience Carotid sinus Nodose Ganglion Azepines Anatomy Hypoxia (medical) Rats medicine.anatomical_structure Endocrinology Control of respiration Respiratory Mechanics Autoradiography Carotid body Neurology (clinical) medicine.symptom |
| Zdroj: | Journal of the Autonomic Nervous System. 53:115-125 |
| ISSN: | 0165-1838 |
| DOI: | 10.1016/0165-1838(94)00179-n |
| Popis: | The effects of ET-1 and ET-3 on ventilation and carotid chemosensory discharge have been studied in rats anaesthetised with pentotarbitone. Autoradiographic studies were also performed in vitro to investigate the binding of [125I]ET-1 to rat carotid body, nodose ganglion and brain stem. ET-1 caused a dose-related hyperventilation that was abolished by cutting both carotid sinus nerves. Recordings of chemosensory discharge from the carotid sinus nerve confirmed that ET-1 caused chemoexcitation. ET-3 had only slight effects. The hyperventilation evoked by ET-1 was antagonised by the ETA receptor antagonist FR139317, but responses to hypoxia (10% oxygen) and to cyanide were unaffected. [125I]ET-1 bound to the carotid body, the nodose ganglion and to the brain stem, particularly in the region of the nucleus tractus solitarii. ET-1 binding in the carotid body was displaceable by FR139317, which is consistent with the functional evidence for ETA receptors in the carotid body. The effects of ET-1 on ventilation, coupled with the presence of ET binding sites in areas involved in respiratory and cardiovascular regulation, is consistent with a physiological role for ET in the control of respiration, but our evidence suggests that ET is not crucial for chemotransduction in acute hypoxia. |
| Databáze: | OpenAIRE |
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