Abstract
The most profound dependence that a higher organism has is its dependence on oxygen. The system mediating the tissue needs of the higher organism for oxygen and the presence of oxygen in the environment is the cardiopulmonary system. The neural control of the anatomical structures of that system includes the carotid body as a receptor. When the organism is challenged by a decrease in the amount of oxygen available to it, which manifests itself in a decrease in the partial pressure of oxygen in the arterial blood, neural activity in the carotid body increases. Among the reflex effects of the carotid body’s increase in neural activity is the increase in tidal volume, breathing frequency, cardiac output, cardiac contractility, and a less precipitous drop in the total peripheral resistance. The carotid body is the essential receptor in the cardiopulmonary system’s response to hypoxia. The question is: “How does it transduce a decrease in low oxygen into increased neural activity? Current speculation postulates that hypoxia somehow depolarizes the neurotransmitter-containing Type I cell, calcium rises in the cytosol from external and perhaps internal sources, promoting the release of one or more excitatory neurotransmitters. The neurotransmitter proceeds to the apposed dendrite, depolarizes it, and the action potential proceeds central to the nucleus tractus solitarius. Subsequently, the cardiopulmonary reflex responses develop.
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References
Boksa, P., and B.G. Livett. Substance P protects against desensitization of the nicotinic response in isolated adrenal chromaffin cells. J. Neurochem. 42: 618–627, 1984.
Douglas, W.W. Is there chemical transmission at chemoreceptors? Pharmacol. Rev. 6: 81–83, 1954.
Eyzaguirre, C., R.S. Fitzgerald, S. Lahiri, and P. Zapata. Arterial chemoreceptors. In: Handbook of Physiology Section2: The Cardiovascular System. Vol III. Peripheral Circulation and Organ Blood Flow. Eds. J.T. Shepherd and F.M. Abboud. Bethesda, Md., American Physiological Society, 1983; pp. 557–622.
Fidone, SJ., and C. Gonzalez. Initiation and control of chemoreceptor activity in the carotid body. In: Handbook of Physiology. Respiration. Vol II. Part 1. Control of Breathing. Eds. N.S. Cherniack and J.G. Widdicombe. Bethesda, Md., American Physiological Society, 1986; pp.247–312.
Heymans, C., and E. Neil. Reflexogenic Areas of the Cardiovascular System. Boston, Little, Brown and Co., 1958.
Heymans, C., and E. Neil. Op. cit., p.191.
Livett, B.G., V. Kozousek, F. Nisobe, and D.M. Dean Substance P inhibits nicotinic activation of chromaffin cells. Nature 278: 256–257, 1979.
Moe, G.K., L R. Capo, and B. Peralta. Action of tetraethylammonium on chemoreceptor and stretch receptor mechanisms. Amer. J. Physiol. 153: 601–605, 1948.
Prabhakar, N.R., J.Mitra, and N.S. Cherniack Role of substance P in hyypercapnic excitation of carotid chemoreceptors. J. Appl. Physiol. 63: 2418–2425, 1987.
Torrance, R.W. Arterial Chemoreceptors. Oxford and Edinburgh, Blackwell Scientific Publications, 1968.
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© 1993 Springer Science+Business Media New York
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Fitzgerald, R.S., Shirahata, M. (1993). Carotid Body Neurotransmission. In: Data, P.G., Acker, H., Lahiri, S. (eds) Neurobiology and Cell Physiology of Chemoreception. Advances in Experimental Medicine and Biology, vol 337. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2966-8_19
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DOI: https://doi.org/10.1007/978-1-4615-2966-8_19
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