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Physiology of O2 Sensing

There are species, developmental, and interorgan differences in metabolic needs and aerobic metabolism that are reflected in species and tissue-specific variations in 02-sensing strategies. However, different species and tissues, faced with similar challenges (e.g., environmental hypoxia) frequently share mechanisms of O2 sensing. A form of hypoxic pulmonary vasoconstriction (HPV), for example, is [Pg.525]

Marcel Dekker, Inc. 270 Madison Avenue. York. New Yoik 10016 [Pg.525]

It is striking that in aU of these O2-sensitive tissues, the effectors appear to be K+ channels (Fig. 2). Isolated PASMCs, ADMCs (or the pheochromocytoma cells, PC 12, used as models for ADMCs), and cells from the CB and NEB respond to hypoxia with a decrease in the outward K+ current (Fig. 2). This results in depolarization of the plasmalemmal membrane, increased opening of voltage-gated Ca + channels, influx of Ca +, and an increase in [Ca +] . In the case of PASMC, this results in the activation of actin-myosin and contraction. In CB glomus cells, it results in release of dopamine from vesicles and increased neural transmission to the brainstem via the IX cranial nerve. Similarly, in ADM and NEB cells K+ current inhibition, membrane depolarization, and increases in [Ca +] cause the release of [Pg.526]

The similarity in the effector mechanism in several of these systems raises the possibility for similarities in the sensor mechanisms. As we discuss below, there is now evidence supporting a role of mitochondria and redox signals in the best-studied 02-sensitive tissues (e.g., the PASMC, DASMC, and the CB type 1 cell). The [Pg.528]


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