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Start Over Descriptor "*CAROTID body" Publisher springer berlin heidelberg
242 results on '"*CAROTID body"'

12. Ultrasound Diagnostics of Neck Masses

Author

Kharchenko, Vladimir P., Kotlyarov, Peter M., Mogutov, Mikhail S., Alexandrov, Yury K., Sencha, Alexander N., Patrunov, Yury N., Belyaev, Denis V., Kharchenko, Vladimir P., Kotlyarov, Peter M., Mogutov, Mikhail S., Alexandrov, Yury K., Sencha, Alexander N., Patrunov, Yury N., and Belyaev, Denis V.

Published
2010
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19. Propofol

Author

Vanlersberghe, C., Camu, F., Starke, K., editor, Schüttler, Jürgen, editor, and Schwilden, Helmut, editor

Published
2008
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21. Carotid body tumour

Author

Benedetti Valentini, Fabrizio, Massa, Rita, Laurito, Antonella, Arnold, Wolfgang, editor, Ganzer, Uwe, editor, Liapis, Christos D., editor, Balzer, Klaus, editor, Benedetti-Valentini, Fabrizio, editor, and Fernandes e Fernandes, José, editor

Published
2007
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24. β-Adrenoceptor blockade prevents carotid body hyperactivity and elevated vascular sympathetic nerve density induced by chronic intermittent hypoxia

Author

Lily L. Cao, Prem Kumar, Jiarong Fu, Abdulaziz A. Alzahrani, Demitris Nathanael, Keith L. Brain, Andrew M. Coney, Hayyaf S. Aldossary, Clare J. Ray, and Andrew P. Holmes

Subjects
Male, medicine.medical_specialty, Sympathetic Nervous System, Physiology, Clinical Biochemistry, Adrenergic beta-Antagonists, Stimulation, Blood Pressure, Propranolol, Drug Administration Schedule, Adrenaline, 03 medical and health sciences, Beta-blockers, 0302 clinical medicine, Chronic intermittent hypoxia, Physiology (medical), Internal medicine, Integrative Physiology, medicine, Animals, Rats, Wistar, Receptor, Hypoxia, 030304 developmental biology, 0303 health sciences, Carotid Body, business.industry, Hypoxia (medical), Carbon Dioxide, Molecular medicine, β-Adrenoceptors, 3. Good health, Rats, Endocrinology, medicine.anatomical_structure, Blood pressure, Hypertension, Immunohistochemistry, Carotid body, Vascular sympathetic nerves, Receptors, Adrenergic, beta-2, medicine.symptom, Receptors, Adrenergic, beta-1, business, 030217 neurology & neurosurgery, medicine.drug
Abstract

Carotid body (CB) hyperactivity promotes hypertension in response to chronic intermittent hypoxia (CIH). The plasma concentration of adrenaline is reported to be elevated in CIH and our previous work suggests that adrenaline directly activates the CB. However, a role for chronic adrenergic stimulation in mediating CB hyperactivity is currently unknown. This study evaluated whether beta-blocker treatment with propranolol (Prop) prevented the development of CB hyperactivity, vascular sympathetic nerve growth and hypertension caused by CIH. Adult male Wistar rats were assigned into 1 of 4 groups: Control (N), N + Prop, CIH and CIH + Prop. The CIH paradigm consisted of 8 cycles h−1, 8 h day−1, for 3 weeks. Propranolol was administered via drinking water to achieve a dose of 40 mg kg−1 day−1. Immunohistochemistry revealed the presence of both β1 and β2-adrenoceptor subtypes on the CB type I cell. CIH caused a 2–3-fold elevation in basal CB single-fibre chemoafferent activity and this was prevented by chronic propranolol treatment. Chemoafferent responses to hypoxia and mitochondrial inhibitors were attenuated by propranolol, an effect that was greater in CIH animals. Propranolol decreased respiratory frequency in normoxia and hypoxia in N and CIH. Propranolol also abolished the CIH mediated increase in vascular sympathetic nerve density. Arterial blood pressure was reduced in propranolol groups during hypoxia. Propranolol exaggerated the fall in blood pressure in most (6/7) CIH animals during hypoxia, suggestive of reduced sympathetic tone. These findings therefore identify new roles for β-adrenergic stimulation in evoking CB hyperactivity, sympathetic vascular hyperinnervation and altered blood pressure control in response to CIH.

Published
2020

25. P1 Receptors in the Respiratory System

Author

Biaggioni, I., Feoktistov, I., Born, G. V. R., editor, Ganten, D., editor, Herken, H., editor, Starke, K., editor, Taylor, P., editor, Abbracchio, Maria Pia, editor, and Williams, Michael, editor

Published
2001
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36. Carcinoid

Author

Order, Stanley E., Donaldson, Sarah S., Order, Stanley E., and Donaldson, Sarah S.

Published
1990
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38. Thymic Mass/Cyst

Author

Arnold, M., Kilborn, T., Andronikou, Savvas, editor, Alexander, Angus, editor, Kilborn, Tracy, editor, Millar, Alastair J. W., editor, and Daneman, Alan, editor

Published
2010
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39. Concluding remarks

Author

Blaustein, M. P., editor, Creutzfeldt, O., editor, Grunicke, H., editor, Habermann, E., editor, Neurath, H., editor, Numa, S., editor, Pette, D., editor, Sakmann, B., editor, Schweiger, M., editor, Trendelenburg, U., editor, Ullrich, K. J., editor, Wright, E. M., editor, Seifert, Roland, and Schultz, Günter

Published
1991
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46. TASK channels in arterial chemoreceptors and their role in oxygen and acid sensing

Author

Buckler, Keith J.

Subjects
K2P channel, Invited Review, Physiology, Clinical Biochemistry, TASK channel, Oxygen sensing, Chemoreceptor Cells, Membrane Potentials, Oxygen, Carotid body, Potassium Channels, Tandem Pore Domain, Physiology (medical), Animals, Humans, Calcium, Potassium channel, Hypoxia, Acidosis
Abstract

Arterial chemoreceptors play a vital role in cardiorespiratory control by providing the brain with information regarding blood oxygen, carbon dioxide, and pH. The main chemoreceptor, the carotid body, is composed of sensory (type 1) cells which respond to hypoxia or acidosis with a depolarising receptor potential which in turn activates voltage-gated calcium entry, neurosecretion and excitation of adjacent afferent nerves. The receptor potential is generated by inhibition of Twik-related acid-sensitive K+ channel 1 and 3 (TASK1/TASK3) heterodimeric channels which normally maintain the cells’ resting membrane potential. These channels are thought to be directly inhibited by acidosis. Oxygen sensitivity, however, probably derives from a metabolic signalling pathway. The carotid body, isolated type 1 cells, and all forms of TASK channel found in the type 1 cell, are highly sensitive to inhibitors of mitochondrial metabolism. Moreover, type1 cell TASK channels are activated by millimolar levels of MgATP. In addition to their role in the transduction of chemostimuli, type 1 cell TASK channels have also been implicated in the modulation of chemoreceptor function by a number of neurocrine/paracrine signalling molecules including adenosine, GABA, and serotonin. They may also be instrumental in mediating the depression of the acute hypoxic ventilatory response that occurs with some general anaesthetics. Modulation of TASK channel activity is therefore a key mechanism by which the excitability of chemoreceptors can be controlled. This is not only of physiological importance but may also offer a therapeutic strategy for the treatment of cardiorespiratory disorders that are associated with chemoreceptor dysfunction.

Published
2015

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