https://uvadoc.uva.es/handle/10324/43679 2026-04-14T16:36:23Z 2026-04-14T16:36:23Z Pérez García, María Teresa López López, José Ramón González Martínez, Constancio https://uvadoc.uva.es/handle/10324/25773 2025-03-03T10:20:44Z 1999-01-01T00:00:00Z

La función principal del aparato respiratorio es mantener las presiones parciales normales de02 y C02 junto con la concentración de H•. Esta importante fun­ ción reguladora constituye la función homeostática del sistema respiratorio, y se consigue ajustando la ventilación a las necesidades metabólicas de consumo de 02 y producción de C02 del organismo. A pesar de las amplias variaciones en los requerimientos de cap­ tación de 02 y eliminación de C021 la P02 y la PC02 arteriales se mantienen normalmente dentro de unos márgenes muy estrechos,debido a la existencia de una regulación compleja de la ventilación mediante una je­ rarquía de sistemas de control. Además,el aparato res­ piratorio participa en otras funciones no homeostáti­ cas (o funciones conductuales) de carácter voluntario, tales como la fonación.

1999-01-01T00:00:00Z López López, José Ramón Peers, Chris https://uvadoc.uva.es/handle/10324/25086 2021-06-24T07:37:04Z 1997-01-01T00:00:00Z

The carotid body (CB) chemoreceptor cells, m spite of their neural origin, were considered nonexcitable until the late 1980's. The remarkable complexity of the organ, together . with the small size of type I cells, represented a limitation for conventional intracellular microelectrode recordings, making a definitive electrophysiological study problematic. The neurochemical approach used during the early l980's, following the stimulus-secretion model established in other neurosecretory systems, suggested an important role for the plasma membrane of type I cells in the hypoxic chemotransduction process. Development of iso­ lated type I cell cultures, together with the use of the patch-damp technique, have brought direct evidence in support of this idea.1 We now have a general picture about the electrical properties of these cells, and their excitable character is unequivocally established; they pos­ sess voltage-dependent ion channels and they are capable of firing action potentials.Al­ though there is a general agreement in the literature about the basic facts, the details are far from being clear. The role of ionic currents in the transduction process by type I cells has been a matter of discussion, and differences in the results reported by different laboratories are evident. In most of the cases the differences could be interpreted on basis of the fact that . either cells from different species or at different stages of development have been studied, but in sorne cases, the differences have led to the proposal of different hypotheses about the mechanisms of chemotransduction.

1997-01-01T00:00:00Z Obeso Cáceres, Ana María de la Luz Rocher Martín, María Asunción López López, José Ramón González Martínez, Constancio https://uvadoc.uva.es/handle/10324/25055 2025-03-03T10:26:56Z 1996-01-01T00:00:00Z

The pívotal role of íntracellular free [Ca2+] fluctuatíons in the control of cellular functíons such as contraction and secretíon, íncludíng the release of neurotransmítters, was recognized many decades ago (see Rubín, 1982). More recently, the list of cellular functíons tríggered or modulated by the levels of Ca2+¡ has grown enormously. Addítional functíons regulated by [Ca2+)¡ include neuronal excítabílity, synaptic plastícíty, gene ex­ pressíon, cellular metabolísm, cell dívísíon and dífferentíatíon, and programmed cell dead (Míller, 1991; Clapham, 1995). Parallelíng the growth in this líst of Ca2+-controlled func­ tíons, a multíplicity of cellular mechanísms aimed at maintaining resting free [Ca2+)¡ in the range of l 00 nM for most cells has been described, allowing increases in Ca2+¡ levels that are specific in their magnitude, time course and spatial distributíon, accordíng to the cell function activated (Toescu, 1995). Since Ca2+ cannot be metabolized, cells regulate theír cytoplasmic levels of free Ca2+ through numerous bínding proteíns and influx and efflux mechanisms (Fíg 1). Ca2+ ínflux to cell cytoplasm from the extracellular milieu occurs vía voltage or receptor operated channels or vía yet ill-defined capacítatíve pathways; the Na+/Ca 2+ exchanger can also produce in sorne círcumstances net ínflux of Ca2+ (Míller, 1991; Clapham, 1995). Ca2+ ef­ flux to the extracellular space occurs against electrochemical gradíents, and thereby the pumpíng out of Ca2+ is directly (Caz+ pump) or indirectly (Na+/Ca2+) coupled to the hy­ drolysis of ATP.

1996-01-01T00:00:00Z González Martínez, Constancio Rocher Martín, María Asunción Obeso Cáceres, Ana María de la Luz López López, José Ramón García-Sancho Martín, Francisco Javier https://uvadoc.uva.es/handle/10324/24947 2025-03-03T10:18:03Z 1993-01-01T00:00:00Z

The carotid body (CB) was defined as a sensory organ by De Castro in 1928. Two years later, Heymanns and coworkers demostrated that the organ was sensitive to alterations in blood gases and pH, in such a way that a decrease in blood P02 or pH or an increase in blood PC02 produced activation of the CB and, reflexely, hyperventilation. De Castro postulated that glomus cells were the sensor structures and that they should release sorn substance to transmit the stimulus to the sensory nerve endings (De Castro, 1928). De Castro's point of view, was widely accepted, and therefore the CB was considered a secondary sensory receptor. As a consequence, the principal aims of many workers in the chemoreception field have been to define the nature of the sensing mechanims ( sensory transduction process ) and to identify the substances released by chern cells.

1993-01-01T00:00:00Z González Martínez, Constancio Rocher Martín, María Asunción Obeso Cáceres, Ana María de la Luz López López, José Ramón López Barneo, José Herreros Guilarte, Benito https://uvadoc.uva.es/handle/10324/24835 2025-03-03T10:27:36Z 1990-01-01T00:00:00Z

Tbe receptor complex in the carotid body (CB) is formed by clusters of type 1 cells that are connected synaptically to the endings of the chemo­ sensory fibers of the carotid sinus nerve (CSN), partia lly covered by type JI cells, and surrounded by a dense net of fenestrated capillaries (1). Sorne aspects of CB chemoreceptor physiology such as the identity of adequate stimulus, the characteristics of the receptor response to the dif­ ferent stimuli, and the reflex responses elicited upon CB stimulation are well known. Contrary to this, the basic mechanisms operating in this re­ ceptor are not completely understood (2). It has been proposed that low Po2 will decrease the ATP leveIs in the chemoreceptor or type 1cells and that this decrease in ATP will trigger the release of neurotransm itters capable of activating the sensory nerve endings. However, there is no proposal on how the decrease in ATP levels can activate the release process. It has been proposed also that high Pco2 and/or low pH in blood will increase the intracellular H+ concentration and that it will result i n in­ creased intracellu lar Ca2 + in type 1 cells and in the release of transmitters. Once again , there is no proposal on the mechanisms by which the increase in H+ can produce the increased Ca2+ concentration in type I cells (2,3).

1990-01-01T00:00:00Z