Ventilatory response to hypoxia in rats: gender differences

Mortola, Jacopo P.; Saiki, Chikako

doi:10.1016/0034-5687(96)00064-3

Cited by 81 publications

(60 citation statements)

References 18 publications

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“…ERa, ERb, and the androgen receptor are expressed in respiratory motor neurons of male and female rats (21) and intraventricular infusion of an ERa antisense vector was shown to decrease brain ERa protein levels and to affect ventilation in rats of both sexes (22). Mortola and Saiki found that conscious adult female rats have a greater hyperventilatory response than males to hypoxia; of note, this observation also was made in studies conducted with ovariectomized females and with prepubertal rats, suggesting that the difference was not mediated by ovarian hormones (23). Significantly increased tidal volume and minute expiratory ventilation, reduced arterial PCO 2 , and enhanced ventilatory response to CO 2 inhalation were observed in male rats after combined administration of a synthetic potent progestin and estradiol for 5 days (24).…”

Section: Sex Differences In Respiratory Physiologymentioning

confidence: 63%

Hormonal Influences on Lung Function and Response to Environmental Agents: Lessons from Animal Models of Respiratory Disease

Card¹,

Zeldin²

2009

Proceedings of the American Thoracic Society

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Numerous studies in humans and experimental animals have identified considerable sex differences in respiratory physiology and in the response of the lung to environmental agents. These differences appear to be mediated, at least in part, by sex hormones and their nuclear receptors. Moreover, animal models are increasingly used to study pathogenic mechanisms and test potential therapies for a variety of human lung diseases, many of which appear to be influenced by sex and sex hormones. In this article, data are summarized from studies of lung function and disease in which sex differences have been observed. Specific attention is paid to animal models of acute lung injury, nonallergic and allergic lung inflammation, and lung fibrosis. It is anticipated that continued investigation of the role of sex and sex hormones in animal models will provide valuable insight into the pathogenesis and potential treatments for a variety of acute and chronic human lung diseases.

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Section: Sex Differences In Respiratory Physiologymentioning

confidence: 63%

Hormonal Influences on Lung Function and Response to Environmental Agents: Lessons from Animal Models of Respiratory Disease

Card¹,

Zeldin²

2009

Proceedings of the American Thoracic Society

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“…Exposure to hypoxia induces both ventilatory changes and a decrease in oxygen consumption (36). The hypoxia-induced ventilatory response is time-dependent, consisting of an immediate increase followed by depression of respiratory drive and further slow recovery upon long-term hypoxic exposure (8,32).…”

Section: Discussionmentioning

confidence: 99%

Task2 potassium channels set central respiratory CO ₂ and O ₂ sensitivity

Gestreau

Heitzmann

Thomas

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

137

140

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Task2 K + channel expression in the central nervous system is surprisingly restricted to a few brainstem nuclei, including the retrotrapezoid (RTN) region. All Task2-positive RTN neurons were lost in mice bearing a Phox2b mutation that causes the human congenital central hypoventilation syndrome. In plethysmography, Task2 −/− mice showed disturbed chemosensory function with hypersensitivity to low CO 2 concentrations, leading to hyperventilation. Task2 probably is needed to stabilize the membrane potential of chemoreceptive cells. In addition, Task2 −/− mice lost the long-term hypoxia-induced respiratory decrease whereas the acute carotid-body-mediated increase was maintained. The lack of anoxia-induced respiratory depression in the isolated brainstemspinal cord preparation suggested a central origin of the phenotype. Task2 activation by reactive oxygen species generated during hypoxia could silence RTN neurons, thus contributing to respiratory depression. These data identify Task2 as a determinant of central O 2 chemoreception and demonstrate that this phenomenon is due to the activity of a small number of neurons located at the ventral medullary surface.breathing | central chemoreceptors | K2P | KCNK5 | ventral medullary surface S pontaneous breathing requires feedback controls in which detection of blood gases and pH is critical. At present, there is good understanding of the brainstem topology of respiratory centers, and functional measurements in vitro and in vivo have revealed the basic principles of the neuronal network required for respiratory rhythmogenesis and pattern generation. This network comprises several groups of respiratory neurons forming columns extending from the caudal ventrolateral medulla to the dorsolateral pons (1, 2). The activity of this network must be stable yet permanently adjusted to variations of O 2 , CO 2 , and pH during diverse physiological conditions, e.g., sleep, exercise, or high altitude (3). The precise physiological processes by which pH, CO 2 , and O 2 changes are sensed and translated into the appropriate respiratory neural output are important mechanisms that are still a matter of debate (4, 5). Changes in arterial CO 2 / pH are detected by peripheral chemoreceptors, mainly carotid bodies, and multiple chemoreceptive areas within the brainstem. Among the central chemoreceptive areas, two have attracted most attention: the raphe nuclei and the retrotrapezoid nucleus (RTN) (6, 7). The carotid bodies are the major sensors for acute O 2 changes. However, for longer periods of hypoxia, respiratory adaptation is substantially mediated by central mechanisms (8). The ventrolateral medullary surface comprising the RTN and the parafacial respiratory group (pFRG) has been proposed to contain intrinsically CO 2 -and O 2 -sensing neurons (9-12). Recently, a mouse model that carries a mutation of the transcription factor Phox2b, which causes congenital central hypoventilation syndrome in humans, was engineered. A specific loss of a population of Phox2b-expressing RTN/pFRG neurons ...

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“…One study showed that conscious adult female rats have a greater hyperventilatory response to hypoxia than males, an effect that did not appear to be mediated by ovarian hormones as the effect was still present in ovariectomized females and in prepubertal rats (48). In the male rat, combined administration of a synthetic potent progestin and estradiol for 5 days significantly increased tidal volume and minute expiratory ventilation, reduced arterial PCO 2 , and enhanced the ventilatory response to CO 2 inhalation (75).…”

Section: Lung and Airway Physiologymentioning

confidence: 99%

The impact of sex and sex hormones on lung physiology and disease: lessons from animal studies

Carey¹,

Card²,

Voltz³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

201

144

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Numerous animal studies have revealed significant effects of sex and sex hormones on normal lung development, lung physiology, and various lung diseases. The primary goal of this review is to summarize knowledge to date on the effects of sex and sex hormones on lung development, physiology, and disease in animals. Specific emphasis will be placed on fibrosis, allergic airway disease, acute lung injury models, respiratory infection, and lung toxicology studies.

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Ventilatory response to hypoxia in rats: gender differences

Cited by 81 publications

References 18 publications

Hormonal Influences on Lung Function and Response to Environmental Agents: Lessons from Animal Models of Respiratory Disease

Hormonal Influences on Lung Function and Response to Environmental Agents: Lessons from Animal Models of Respiratory Disease

Task2 potassium channels set central respiratory CO ₂ and O ₂ sensitivity

The impact of sex and sex hormones on lung physiology and disease: lessons from animal studies

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Ventilatory response to hypoxia in rats: gender differences

Cited by 81 publications

References 18 publications

Hormonal Influences on Lung Function and Response to Environmental Agents: Lessons from Animal Models of Respiratory Disease

Hormonal Influences on Lung Function and Response to Environmental Agents: Lessons from Animal Models of Respiratory Disease

Task2 potassium channels set central respiratory CO 2 and O 2 sensitivity

The impact of sex and sex hormones on lung physiology and disease: lessons from animal studies

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Task2 potassium channels set central respiratory CO ₂ and O ₂ sensitivity