Regulation of oxygen sensing by ion channels

Abstract

O(2) sensing is of critical importance for cell survival and adaptation of living organisms to changing environments or physiological conditions. O(2)-sensitive ion channels are major effectors of the cellular responses to hypoxia. These channels are preferentially found in excitable neurosecretory cells (glomus cells of the carotid body, cells in the neuroepithelial bodies of the lung, and neonatal adrenal chromaffin cells), which mediate fast cardiorespiratory adjustments to hypoxia. O(2)-sensitive channels are also expressed in the pulmonary and systemic arterial smooth muscle cells where they participate in the vasomotor responses to low O(2) tension (particularly in hypoxic pulmonary vasoconstriction). The mechanisms underlying O(2) sensing and how the O(2) sensors interact with the ion channels remain unknown. Recent advances in the field give different support to the various current hypotheses. Besides the participation of ion channels in acute O(2) sensing, they also contribute to the gene program developed under chronic hypoxia. Gene expression of T-type calcium channels is upregulated by hypoxia through the same hypoxia-inducible factor-dependent signaling pathway utilized by the classical O(2)-regulated genes. Alteration of acute or chronic O(2) sensing by ion channels could participate in the pathophysiology of human diseases, such as sudden infant death syndrome or primary pulmonary hypertension.

Vasodilation induced by oxygen/glucose deprivation is attenuated in cerebral arteries of SUR2 null mice

“…This reaction, termed the "myogenic response," is important for systemic blood pressure regulation and circulatory blood flow autoregulation and provides resting arterial tone that can be altered by vasoconstrictors or vasodilators (9). The response of blood vessels to changes in oxygen partial pressure depends on the anatomical origin of the vasculature (21). Hypoxia dilates cerebral and systemic arteries and arterioles but constricts small distal pulmonary arteries and arterioles (23,30).…”

Transcriptional and post-transcriptional regulation of gene expression in submerged root cells of maize

“…3,4 Physiologically, alteration of metabolic pathways results in a change of cytosolic pH, accumulation of ROS and hormone homeostasis. [5][6][7][8] Adaptation also occurs via a wide variety of morphological and anatomical responses to oxygen limitation of roots or entire plants, including formation of aerenchyma, fast underwater elongation of shoots or leaves, stomatal closure, adventitious root formation and lateral root development. 3,[9][10][11] Each of these reactions is mediated by plant hormones, such as ethylene, auxin and ABA.…”

Canaux potassiques et physiologie de l’épithélium respiratoire

“…Ce canal de petite conductance (< 3pS, pS pour picosiemens), activé par l'AMPc, participe pour une large part au courant K + basolatéral mesuré en chambre de Ussing [11,13], mais il pourrait également être exprimé à la membrane apicale [15] [34]. Toutefois, la sensibilité à l'O 2 pourrait ne pas être intrinsèque au canal mais dépendre d'autres molécules telles que les espèces réactives de l'O 2 (ROS) produites par la NADPH oxydase et/ou la mitochondrie [31,33]. Les canaux K + sensibles à l'O 2 pourraient donc contribuer à la fonction d'adaptation du poumon à son environnement et il a été proposé que leur altération participe à la pathophysiologie de l'hypertension pulmonaire [33].…”

“…Toutefois, la sensibilité à l'O 2 pourrait ne pas être intrinsèque au canal mais dépendre d'autres molécules telles que les espèces réactives de l'O 2 (ROS) produites par la NADPH oxydase et/ou la mitochondrie [31,33]. Les canaux K + sensibles à l'O 2 pourraient donc contribuer à la fonction d'adaptation du poumon à son environnement et il a été proposé que leur altération participe à la pathophysiologie de l'hypertension pulmonaire [33]. Les différen-tes étapes de la réparation de l'épithélium respiratoire consécutive à des lésions sont schématisées en A.…”