Prolegomena

Torrance, R. W.

doi:10.1007/978-1-4615-5891-0_2

Cited by 24 publications

(1 citation statement)

References 32 publications

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“…Podría argumentarse que la acidificación intracelular reduciría la afinidad de la maquinaria exocitótica por el Ca 2+ , con lo que, a pesar del aumento relativamente alto de la concentración intracelular de Ca 2+, la respuesta secretora sea pequeña. Sin embargo, esta posibilidad contradice la potenciación de respuestas que se observa entre los estímulos hipóxicos y ácidos [129]. Finalmente, aunque la gran sensibilidad del maxi-K a la acidificación intracelular [130] es congruente con la despolarización que producen los estímulos ácidos en las células quimiorreceptoras, el TASK-1 es sensible al pH extracelular [93] y, según hemos comentado, los ácidos débiles, incluido el propio CO 2 , producen un aumento del Ca 2+ intracelular aun con un pH extracelular de 7,40 [125,126].…”

Section: Mecanismos De Transducción Del Estímulo Hipóxicounclassified

Quimiorreceptores arteriales: mecanismos celulares y moleculares de las funciones adaptativa y homeostática del cuerpo carotídeo

González

Rocher²,

Zapata³

2003

RevNeurol

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The carotid body is a sensory chemoreceptor organ located in the vicinity of the carotid bifurcation. Structurally it is composed of cell clusters formed by chemoreceptor and supporting cells. The sensory nerve endings of the carotid sinus nerve penetrate the clusters to synapse with chemoreceptor cells. The carotid body plays an important role in the control of ventilation during hypoxia, hypercapnia and acidosis. Hypoxia and other natural stimuli are detected by chemoreceptor cells which upon stimulation increase their rate of release of neurotransmitters. Neurotransmitters in turn increase the action potential frequency in the carotid sinus nerve which via its central projections to the brainstem activates ventilation. This review is devoted to the cellular aspects of the function of this chemoreceptor organ. From a brief description of the complex structure of the carotid body, we go to present a summary of the main prevailing theories concerning the transduction mechanisms for hypoxic and acidic/ hypercapnic stimuli, with special emphasis on the electrical properties of cultured chemoreceptors cells. A special attention is provided to the possible significance of reactive oxygen species as mediators of the hypoxic transduction cascade. The neurotransmission between chemoreceptor cells and the sensory nerve endings is also covered in certain detail. After a brief historical presentation of the theories of communication between these two structures, we examine, following the classical criteria of neurotransmission, the functional significance of acetylcholine, dopamine, substance P and other neurotransmitters known to be present in chemoreceptor cells.

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Section: Mecanismos De Transducción Del Estímulo Hipóxicounclassified

Quimiorreceptores arteriales: mecanismos celulares y moleculares de las funciones adaptativa y homeostática del cuerpo carotídeo

González

Rocher²,

Zapata³

2003

RevNeurol

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Exercise Hyperpnea

Ward

2006

Wiley Encyclopedia of Biomedical Engineering

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Control schemes of ventilation during moderate exercise [i.e., below the lactate threshold ( θ L )] have classically incorporated both proportional humoral feedback (carotid and central chemoreflex) and neurogenic feed forward (central command, muscle, cardiocirculatory) to provide stability of arterial PCO 2 (PaCO 2 ) pH (pHa), and PO 2 (PaO 2 ). In response to a step work‐rate (WR) forcing from prior rest in the upright posture, increases abruptly for some 15–20 s, this being followed by a subsequent more‐prominent exponential component (consistent with first‐order kinetics). The lack of any sustained error signals in the mean levels of PaCO 2 , pHa, or PaO 2 , coupled with the dynamic matching of with pulmonary CO 2 output but not O 2 uptake or WR, suggests that the controller operates as if it incorporates an errorless humoral feedback element proportional to (or some close proxy). In addition, the controller seems to evidence considerable redundancy, with particular sensory deficits having little effect on the steady‐state response to exercise or the stability of PaCO 2 between rest and exercise. Above θ L , kinetics become markedly nonlinear, with steady states being either delayed or not attained, which reflects the influence of the developing metabolic acidemia (1) indirectly, via bicarbonate‐mediated body CO 2 stores washout, which augments ; and (2) directly, to effect respiratory compensation for the falling pHa (this being constrained by the falling PaCO 2 that results from increasing out of proportion to ). The carotid bodies are important in mediating this respiratory compensation, although with surprisingly slow kinetics, In conclusion, despite there now being general agreement regarding the overall characteristics of the response to exercise, the precise details of the control process(es) remain unresolved.

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Are there gap junctions between chief (glomus, type I) cells in the carotid body chemoreceptor? A review

Kondo

2002

Microscopy Res & Technique

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Since the dye- and electronic couplings between the carotid body chief cells have been demonstrated, the detection and localization of the gap junctions in the carotid body is crucial to understanding the functional mechanism of chemoreception. However, conventional electron microscopy has been unsuccessful in unquestionably detecting ultrastructural features equivalent to the gap junctions, such as close (2 nm in width) membrane appositions in ultrathin sections and aggregations of intramembranous particles in freeze-fracture replicas of the carotid body. We previously reported using a modified electron microscopic study by chemically fixed and subsequent rapid freezing and freeze-substitution method a number of close membrane appositions comparable to the gap junctions. However, we later found that the freeze-substitution also induces numerous close apposition of the membrane in sites where the gap junctions are not known to occur, indicating that the modified electron microscopy by freeze-substitution is not always confirmative in the detection of the gap junction. With regard to the molecular evidence for the gap junction in the carotid body, there have so far been few data on the immunohistochemical demonstration on connexin 32 and 43 in cultured chief cells, but not in the in situ cells.

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Prolegomena

Cited by 24 publications

References 32 publications

Quimiorreceptores arteriales: mecanismos celulares y moleculares de las funciones adaptativa y homeostática del cuerpo carotídeo

Quimiorreceptores arteriales: mecanismos celulares y moleculares de las funciones adaptativa y homeostática del cuerpo carotídeo

Exercise Hyperpnea

Are there gap junctions between chief (glomus, type I) cells in the carotid body chemoreceptor? A review

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