Postnatal maturation of carotid body and type I cell chemoreception in the rat

Bamford, Owen S.; Sterni, Laura M.; Wasicko, M. J.; Montrose, Marshall H.; Carroll, John L.

doi:10.1152/ajplung.1999.276.5.l875

Cited by 43 publications

(48 citation statements)

References 27 publications

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“…The mechanism by which D2 receptor stimulation decreases the [ ] i response to hypoxia increased with age, consistent with our previous reports in developing rabbits and rats (6,41,45), and age-related changes in the effects of quinpirole were also evident. Quinpirole had a minimal effect on the [Ca 2ϩ ] i response to 0% O 2 in the 1-day-old group.…”

Section: Discussionsupporting

confidence: 91%

Dopamine D2 receptor modulation of carotid body type 1 cell intracellular calcium in developing rats

Carroll

Boyle

Wasicko

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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]i) response to hypoxia in type 1 cells from 1, 3, and 11-to 16-day-old rats. Using fura-2, we studied the effects of quinpirole, a D2 receptor agonist, on type 1 cell [Ca 2ϩ ]i response to 90-s hypoxia challenges (PO2 ϳ1-2 mmHg). Cells were sequentially exposed to the following challenges: 1) hypoxia control, 2) hypoxia plus quinpirole, and 3) hypoxia plus quinpirole plus sulpiride (D2 receptor antagonist). In the 11-to 16-day-old group, type 1 cell [Ca 2ϩ ]i increased ϳ3 to 4-fold over resting [Ca 2ϩ ]i in response to hypoxia. Quinpirole (10 M) significantly blunted the peak [Ca 2ϩ ]i response to hypoxia. Repeat challenge with hypoxia plus 10 M quinpirole in the presence of 10 M sulpiride partially restored the hypoxia [Ca 2ϩ ]i response. In sharp contrast to the older aged group, 10 M quinpirole had minimal effect on hypoxia response of type 1 cells from 1-day-olds and a small but significant effect at 3 days of age. We conclude that stimulation of dopamine D2 receptors inhibits type 1 cell [Ca 2ϩ ]i response to hypoxia, consistent with an inhibitory autoreceptor role. These findings suggest dopamine-mediated inhibition and oxygen sensitivity increase with age on a similar time course and do not support a role for dopamine as a major mediator of carotid chemoreceptor resetting. dopamine receptors; hypoxia; development; chemoreceptor THE MAIN SENSORS of arterial oxygen level in mammals are the carotid body (CB) chemoreceptors (25). It is widely believed that hypoxia leads to CB type 1 cell depolarization and Ca 2ϩ influx through voltage-gated calcium channels. The rise in intracellular calcium ([Ca 2ϩ ] i ) releases neurotransmitter(s), which are believed to cause firing of action potentials in the adjacent carotid sinus nerve terminals and to act presynaptically on type 1 cell autoreceptors (25). Carotid sinus nerve (CSN) input to brain stem respiratory control nuclei drives the ventilatory response to hypoxia and mediates, at least in part, other defensive responses to hypoxic stress (12, 13, 21-23, 30, 31).In neonates, but not adults, carotid denervation leads to high mortality rates and abnormalities of respiratory control (13,15,18,30,31), suggesting a vulnerable period during mammalian postnatal maturation during which the CB is important for survival and normal maturation of breathing control. Despite their importance in the developing infant, the carotid chemoreceptors have low sensitivity to hypoxia at birth and become more sensitive over the first few days or weeks of life (9,10,14,17,33,36,38), a process termed "resetting." The mechanism(s) underlying resetting are unknown, but some have postulated involvement of inhibitory neuromodulators such as dopamine (DA) (28,29).In rats and rabbits, an age-related increase in O 2 sensitivity occurs at the type 1 cell level (41, 45). Both the [Ca 2ϩ ] i rise and the neurotransmitter (catecholamine) release in response to hypoxia increase with maturation, exhibiting the same time course as CSN response maturation, strongly suggesting that a s...

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Section: Discussionsupporting

confidence: 91%

Dopamine D2 receptor modulation of carotid body type 1 cell intracellular calcium in developing rats

Carroll

Boyle

Wasicko

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The CO 2 response of the isolated carotid body is present in young animals and generally equal to the adult response. The multiplicative interaction between hypercapnia and hypoxia increases over the course of development, but the intrinsic CO 2 sensitivity of the carotid body under normoxic conditions does not vary much as a function of age (Pepper et al, 1995;Calder et al, 1997;Bamford et al, 1999). The contribution of peripheral chemoreceptors to the normoxic hypercapnic ventilatory response in intact animals is stable in the neonatal period of development in humans as well, but the interactive effects of CO 2 -O 2 at the carotid body seem to increase as babies mature (Søvik and Lossius, 2004).…”

Section: Differential Maturation Between Peripheral Versus Central Chmentioning

confidence: 99%

Neonatal maturation of the hypercapnic ventilatory response and central neural CO2 chemosensitivity

Putnam

Conrad

Gdovin

et al. 2005

Respiratory Physiology & Neurobiology

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The ventilatory response to CO 2 changes as a function of neonatal development. In rats, a ventilatory response to CO 2 is present in the first 5 days of life, but this ventilatory response to CO 2 wanes and reaches its lowest point around postnatal day 8. Subsequently, the ventilatory response to CO 2 rises towards adult levels. Similar patterns in the ventilatory response to CO 2 are seen in some other species, although some animals do not exhibit all of these phases. Different developmental patterns of the ventilatory response to CO 2 may be related to the state of development of the animal at birth. The triphasic pattern of responsiveness (early decline, a nadir, and subsequent achievement of adult levels of responsiveness) may arise from the development of several processes, including central neural mechanisms, gas exchange, the neuromuscular junction, respiratory muscles and respiratory mechanics. We only discuss central neural mechanisms here, including altered CO 2 sensitivity of neurons among the various sites of central CO 2 chemosensitivity, changes in astrocytic function during development, the maturation of electrical and chemical synaptic mechanisms (both inhibitory and excitatory mechanisms) or changes in the integration of chemosensory information originating from peripheral and multiple central CO 2 chemosensory sites. Among these central processes, the maturation of synaptic mechanisms seems most important and the relative maturation of synaptic processes may also determine how plastic the response to CO 2 is at any particular age.

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“…High levels of CO 2 increase the sensitivity of the carotid body chemoreceptors to low O 2 ; conversely, low levels of O 2 increase the sensitivity of the ventilatory response to hypercapnia (Bamford et al, 1999). From a control systems perspective, the PO 2 -chemoreceptor activity curve shifts rightward in the presence of elevated CO 2 levels while hypoxic conditions cause an increase in the slope of the PCO 2 -chemoreceptor activity curve (Lahiri and Delaney, 1975a).…”

Section: Potential Mechanisms Underlying Interactive Effects Between mentioning

confidence: 98%

“…In mammals, interactive effects of O 2 and CO 2 are detectible at the level of ventilation (Nielsen and Smith, 1952), at the level of carotid sinus nerve discharge (Tenney and Brooks, 1966;Daristotle et al, 1987;Lahiri and Delaney, 1975a) and to a very small extent at the level of the increase in intracellular [Ca 2+ ], within the glomus cells, associated with chemoreceptor activation (Bamford et al, 1999;Roy et al, 2000). High levels of CO 2 increase the sensitivity of the carotid body chemoreceptors to low O 2 ; conversely, low levels of O 2 increase the sensitivity of the ventilatory response to hypercapnia (Bamford et al, 1999).…”

Section: Potential Mechanisms Underlying Interactive Effects Between mentioning

confidence: 99%

Reciprocal modulation of O2 and CO2 cardiorespiratory chemoreflexes in the tambaqui

Reid

Perry

Gilmour

et al. 2005

Respiratory Physiology & Neurobiology

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This study examined the effect of acute hypoxic and hypercapnic cardiorespiratory stimuli, superimposed on existing cardiorespiratory disturbances in tambaqui. In their natural habitat, these fish often encounter periods of hypoxic hypercapnia that can be acutely exacerbated by water turnover. Tambaqui were exposed to periods of normoxia, hypoxia, hyperoxia and hypercapnia during which, externally oriented O 2 and CO 2 chemoreceptors were further stimulated, by administration into the inspired water of sodium cyanide and CO 2 -equilibrated water, respectively. Hyperoxic water increased the sensitivity of the NaCN-evoked increase in breathing frequency (f R ) and decrease in heart rate. Hypoxia and hypercapnia attenuated the increase in f R but, aside from blood pressure, did not influence the magnitude of NaCN-evoked cardiovascular changes. Water PO 2 influenced the magnitude of the CO 2 -evoked cardiorespiratory changes and the sensitivity of CO 2 -evoked changes in heart rate and blood flow. The results indicate that existing respiratory disturbances modulate cardiorespiratory responses to further respiratory challenges reflecting both changes in chemosensitivity and the capacity for further change.

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Postnatal maturation of carotid body and type I cell chemoreception in the rat

Cited by 43 publications

References 27 publications

Dopamine D2 receptor modulation of carotid body type 1 cell intracellular calcium in developing rats

Dopamine D2 receptor modulation of carotid body type 1 cell intracellular calcium in developing rats

Neonatal maturation of the hypercapnic ventilatory response and central neural CO2 chemosensitivity

Reciprocal modulation of O2 and CO2 cardiorespiratory chemoreflexes in the tambaqui

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