Cat carotid body chemoreceptor responses before and after nicotine receptor blockade with α-bungarotoxin

Mulligan, E.; Lahiri, S.

doi:10.1016/0165-1838(87)90131-7

Cited by 9 publications

(4 citation statements)

References 17 publications

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“…the hypoxic stimulation was of the same magnitude when nicotine was given alone or after mecamylamine pretreatment. It can thus be inferred from these observations that stimulation of nicotinic receptors does not play a major role in mediating the ventilatory response to hypoxia in the cat (38). Because nicotine has powerful stimulatory effects on peripheral chemoreceptor tonic discharge, but it does not enhance the rise in peripheral chemoreceptor discharge during hypoxia, these two effects may be mediated through separate mechanisms.…”

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confidence: 77%

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Nicotine Attenuates the Ventilatory Response to Hypoxia in the Developing Lamb

et al. 1995

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Decreased ability to generate a hyperventilatory response to hypoxemia is believed to be an important mechanism in the pathophysiology of sudden infant death syndrome, and maternal smoking is a leading risk factor. To investigate whether there may be a link between these two observations, we studied five Iambs at mean ages of 7, 17, and 27 d to determine the effects of an i.v, infusion of nicotine (0.5 j.Lg/kglmin) on ventilation when peripheral chemoreceptor activity was stimulated by hypoxia (0.1 Fi0 2 ) or briefly inhibited by hyperoxia. Ventilatory measurements were performed using a computer-aided occlusion valve device which permitted breath-by-breath determinations of inspiratory occlusion pressures (P0.1) and minute ventilation. Nicotine attenuated the early ventilatory response to hypoxia (min 1, 2, and 3 of the test) by 8, 26, and 37%, respectively, at the age of 7 d (analysis of variance overall, p < 0.05), by 23%, 23 and 37% at 17 d (p = NS) and by 40,45, and 37% at 27 d (p < 0.05). The decrease in ventilation in response to hyperoxia during the control study without nicotine was 18,35, and 34% at 7, 17, and 27 d, respectively. Nicotine caused a greater decrease in the response: 31, 45, and 46%, respectively, (p < 0.05 at 27 d). The paradoxical effects of nicotine, attenuation of the ventilatory response to hypoxia and augmentation of the response to A substantial number of infants who die of SIDS have been reported to have brain stem gliosis (1) and elevated hypoxanthine level s in the vitreous humor (2) , findings suggestive of repeated hypoxemic epi sodes before death. These ob servations, together with reports of altered neurotransmitter content

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confidence: 77%

“…In the adult cat, Mulligan and Lahiri (38) have shown that nicotine augments CB discharge through a direct stimulation via nicotine receptors. This stimulatory effect could be abolished by mecamylamine, a ganglionic-type nicotine receptor blocker.…”

Section: • •mentioning

confidence: 99%

Nicotine Attenuates the Ventilatory Response to Hypoxia in the Developing Lamb

et al. 1995

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“…Despite their importance, the carotid chemoreceptors in neonates exhibit low sensitivity to hypoxia compared with adults and become more sensitive over the first few weeks of life. This process, termed "resetting" of carotid body O 2 sensitivity, occurs in all mammalian species studied to date (8,9,12,20,29,36,37 …”

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confidence: 99%

Postnatal development of E-4031-sensitive potassium current in rat carotid chemoreceptor cells

Kim¹,

Boyle²,

Carroll³

2005

Journal of Applied Physiology

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ϩ currents that inhibit hypoxia-induced depolarization and that a decrease in this current with age could underlie, in part, the developmental increase in type I cell depolarization response to hypoxia. In dissociated type I cells from 0-to 1-and 11-to 16-day-old rats, using perforated patch-clamp and 70 mM K ϩ extracellular solution, we measured repolarization-induced inward K ϩ tail currents in the absence and presence of E-4031, a specific HERG channel blocker. This allowed isolation of the E-4031-sensitive HERG-like current. E-4031-sensitive peak currents in type I cells from 0-to-1-day-old rats were 2.5-fold larger than in cells from 11-to 16-day-old rats. E-4031-sensitive current density in newborn type I cells was twofold greater than in cells from 11-to 16-day-old rats. Under current clamp conditions, E-4031 enhanced hypoxia-induced depolarization in type I cells from 0-to-1-day-old but not 11-to 16-day-old rats. With use of fura 2 to measure intracellular Ca 2ϩ , E-4031 increased the cytosolic Ca 2ϩ concentration response to anoxia in cells from 0-to-1-day-old but not cells from 11-to 16-day-old rats. E-4031-sensitive K ϩ currents are present in newborn carotid body type I cells and decline with age. These findings are consistent with a role for E-4031-sensitive K ϩ current, and possibly HERG-like K ϩ currents, in the type I cell hypoxia response maturation.human ether-a-go-go-related gene; potassium channel; hypoxia THE CAROTID BODY chemoreceptors mediate ventilatory and other defensive responses to hypoxic stress in mammals (11,23,28) and appear to be important for survival during postnatal maturation (14,21,28). Despite their importance, the carotid chemoreceptors in neonates exhibit low sensitivity to hypoxia compared with adults and become more sensitive over the first few weeks of life. This process, termed "resetting" of carotid body O 2 sensitivity, occurs in all mammalian species studied to date (8,9,12,20,29,36,37

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“…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).…”

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confidence: 99%

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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Cat carotid body chemoreceptor responses before and after nicotine receptor blockade with α-bungarotoxin

Cited by 9 publications

References 17 publications

Nicotine Attenuates the Ventilatory Response to Hypoxia in the Developing Lamb

Nicotine Attenuates the Ventilatory Response to Hypoxia in the Developing Lamb

Postnatal development of E-4031-sensitive potassium current in rat carotid chemoreceptor cells

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

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