Hypoxia and acidosis increase the secretion of catecholamines in the neonatal rat adrenal medulla: an in vitro study

Rico, Alberto J.; Prieto‐Lloret, Jesus; González, C.; Rigual, R.

doi:10.1152/ajpcell.00023.2005

Cited by 45 publications

(46 citation statements)

References 44 publications

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“…We showed that at birth, the release of adrenaline was defective in FR50 pups, suggesting that FR50 newborns were likely less sensitive to the stress associated with birth. In addition, it suggests that maternal FR50 impaired the non-neurogenic control of catecholamine release because at this stage, splanchnic control of the adrenal medulla is not yet effective [39,40,41,42]. This is in accordance with the observation that intrauterine growth retardation led to the complete loss of adrenaline synthesis and release in response to hypoxia [43, 44].…”

Section: Discussionsupporting

confidence: 62%

Maternal Perinatal Undernutrition Alters Postnatal Development of Chromaffin Cells in the Male Rat Adrenal Medulla

Molendi-Coste

Laborie²,

Scarpa³

et al. 2009

Neuroendocrinology

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Numerous data suggest that the development of the sympathoadrenal system is highly sensitive to the perinatal environment. We previously reported that maternal perinatal food restriction by 50% (FR50) altered chromaffin cell (CC) organization and activity in offspring at weaning. This study investigated the effects of FR50 on the postnatal time course of CC functional and structural adaptations. FR50 pups exhibited smaller and more abundant scattered clusters of noradrenergic CCs as early as postnatal day 7 (P7), indicating that morphological changes took place earlier during development. At birth, the adrenaline release was defective in FR50 pups, suggesting that maternal FR50 impaired the non-neurogenic control of catecholamine release. At P4, the catecholamine release in response to insulin-induced hypoglycaemia was also absent in FR50 pups. This was associated with the reduction of adrenal catecholamine contents, indicating that the failure to synthesize catecholamine might lead to impaired secretion. We hypothesized that maternal FR50 accelerated the functional connections between CCs and splanchnic nerve endings, leading to the premature loss of the non-neurogenic response. Acetylcholine-containing synaptic endings seemed more precociously functional in FR50 pups, as suggested by increased levels of acetylcholine esterase activity at P14. At P7, insulin-induced hypoglycaemia caused preferential adrenaline release associated with increased catecholamine contents in both groups. However, the response was accentuated in FR50 pups. At P14, the insulin challenge increased plasma levels of adrenaline in control rats, whereas it markedly enhanced the circulating level of both catecholamines in FR50 pups. We demonstrated that maternal FR50 leads to developmentally impaired noradrenergic CC aggregation and advanced splanchnic neurotransmission maturation associated with altered medulla activity in response to metabolic stress. This might contribute to the long-lasting malprogramming of the adrenal medulla and to the development of chronic adult diseases.

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Section: Discussionsupporting

confidence: 62%

Maternal Perinatal Undernutrition Alters Postnatal Development of Chromaffin Cells in the Male Rat Adrenal Medulla

Molendi-Coste

Laborie²,

Scarpa³

et al. 2009

Neuroendocrinology

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“…2Ai,Bi. Acute hypoxia also induces CAT secretion when applied to fresh tissue slices of the adrenal gland (García-Fernández et al, 2007), and to superfused whole adrenal glands (Adams et al, 1996;Rico et al, 2005) In nicotine-treated AMCs, hypoxia does not affect outward K + current, although hypercapnia still produces significant inhibition at +30 mV. In current-clamp recordings, both hypoxia (Bi) and isohydric hypercapnia (10% CO 2 , pH 7.4; Ci) produce depolarizing excitatory responses in salinetreated AMCs.…”

Section: Mechanisms Of Acute Hypoxia Sensing In Perinatal Amcsmentioning

confidence: 99%

“…Furthermore, they showed in denervation experiments that removal of the splanchnic innervation in mature or adult animals resulted in a gradual re-appearance of this non-neurogenic mechanism (Slotkin and Seidler, 1988). More recent studies in the rat suggest that adrenal responses to hypercapnia, acidity and hypoglycemia are also suppressed postnatally, in parallel with splanchnic innervation (Livermore et al, 2011;Livermore et al, 2012;Muñoz-Cabello et al, 2005;Rico et al, 2005). Interestingly, in mammals that are born relatively mature (e.g.…”

Section: Introductionmentioning

confidence: 99%

Ontogeny of O2 and CO2//H+ chemosensitivity in adrenal chromaffin cells: role of innervation

Salman

Buttigieg

Nurse

2014

Journal of Experimental Biology

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The adrenal medulla plays a key role in the physiological responses of developing and mature mammals by releasing catecholamines (CAT) during stress. In rodents and humans, the innervation of CATproducing, adrenomedullary chromaffin cells (AMCs) is immature or absent during early postnatal life, when these cells possess 'direct' hypoxia-and CO 2 /H + -chemosensing mechanisms. During asphyxial stressors at birth, these mechanisms contribute to a CAT surge that is critical for adaptation to extra-uterine life. These direct chemosensing mechanisms regress postnatally, in parallel with maturation of splanchnic innervation. Here, we review the evidence that neurotransmitters released from the splanchnic nerve during innervation activate signaling cascades that ultimately cause regression of direct AMC chemosensitivity to hypoxia and hypercapnia. In particular, we consider the roles of cholinergic and opioid receptor signaling, given that splanchnic nerves release acetylcholine and opiate peptides onto their respective postsynaptic nicotinic and opioid receptors on AMCs. Recent in vivo and in vitro studies in the rat suggest that interactions involving α7 nicotinic acetylcholine receptors (nAChRs), the hypoxia inducible factor (HIF)-2α signaling pathway, protein kinases and ATP-sensitive K + (K ATP ) channels contribute to the selective suppression of hypoxic chemosensitivity. In contrast, interactions involving μ-and/or δ-opiod receptor signaling pathways contribute to the suppression of both hypoxic and hypercapnic chemosensitivity, via regulation of the expression of K ATP channels and carbonic anhydrase (CA I and II), respectively. These data suggest that the ontogeny of O 2 and CO 2 /H + chemosensitivity in chromaffin cells can be regulated by the tonic release of presynaptic neurotransmitters.

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“…We can name these cells as cells endowed with sensitivity to physiological hypoxia (Gonzalez, 1998). Neonatal adrenal medulla chromaffin cells are also endowed with sensitivity to physiological hypoxia, however they lose their intrinsic O 2 -sensitivity early in postnatal age when adrenal medulla becomes functionally innervated by splanchnic nerves (Seidler and Slotkin, 1985;Rico et al, 2005). Chemoreceptor cells of the airways neuroepithelial bodies also are oxygen sensitive in neonatal animals (Cutz et al, 2009), but become greatly atrophic in adult mammals (Cutz, 1997).…”

Section: The Need For Oxygen Sensing and Transduction Cascadesmentioning

confidence: 99%

A revisit to O2 sensing and transduction in the carotid body chemoreceptors in the context of reactive oxygen species biology

González

Agapito

Rocher

et al. 2010

Respiratory Physiology & Neurobiology

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a b s t r a c tOxygen-sensing and transduction in purposeful responses in cells and organisms is of great physiological and medical interest. All animals, including humans, encounter in their lifespan many situations in which oxygen availability might be insufficient, whether acutely or chronically, physiologically or pathologically. Therefore to trace at the molecular level the sequence of events or steps connecting the oxygen deficit with the cell responses is of interest in itself as an achievement of science. In addition, it is also of great medical interest as such knowledge might facilitate the therapeutical approach to patients and to design strategies to minimize hypoxic damage. In our article we define the concepts of sensors and transducers, the steps of the hypoxic transduction cascade in the carotid body chemoreceptor cells and also discuss current models of oxygen-sensing (bioenergetic, biosynthetic and conformational) with their supportive and unsupportive data from updated literature. We envision oxygen-sensing in carotid body chemoreceptor cells as a process initiated at the level of plasma membrane and performed by a hemoprotein, which might be NOX4 or a hemoprotein not yet chemically identified. Upon oxygen-desaturation, the sensor would experience conformational changes allosterically transmitted to oxygen regulated K + channels, the initial effectors in the transduction cascade. A decrease in their opening probability would produce cell depolarization, activation of voltage dependent calcium channels and release of neurotransmitters. Neurotransmitters would activate the nerve endings of the carotid body sensory nerve to convey the information of the hypoxic situation to the central nervous system that would command ventilation to fight hypoxia.

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Hypoxia and acidosis increase the secretion of catecholamines in the neonatal rat adrenal medulla: an in vitro study

Cited by 45 publications

References 44 publications

Maternal Perinatal Undernutrition Alters Postnatal Development of Chromaffin Cells in the Male Rat Adrenal Medulla

Maternal Perinatal Undernutrition Alters Postnatal Development of Chromaffin Cells in the Male Rat Adrenal Medulla

Ontogeny of O2 and CO2//H+ chemosensitivity in adrenal chromaffin cells: role of innervation

A revisit to O2 sensing and transduction in the carotid body chemoreceptors in the context of reactive oxygen species biology

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