cAMP production in rabbit carotid body:  role of adenosine

Chen, J.; Dinger, B.; Fidone, S.

doi:10.1152/jappl.1997.82.6.1771

Cited by 25 publications

(29 citation statements)

References 28 publications

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“…The normoxic cAMP levels do not differ in the four ages studied, and the pattern of cAMP production in response to different O 2 concentrations remained almost unchanged in old animals. The cAMP levels found in the rat CB in the present study, expressed in unit weight, are nearly identical to the values reported in the rabbit CB (Perez-Garcia et al 1990;Chen et al 1997). At all ages, cAMP levels were maximal in normoxic conditions.…”

Section: Discussionsupporting

confidence: 88%

Carotid body function in aged rats: responses to hypoxia, ischemia, dopamine, and adenosine

Monteiro

Batuca

Obeso

et al. 2010

AGE

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The carotid body (CB) is the main arterial chemoreceptor with a low threshold to hypoxia. CB activity is augmented by A 2 -adenosine receptors stimulation and attenuated by D 2 -dopamine receptors. The effect of aging on ventilatory responses mediated by the CB to hypoxia, ischemia, and to adenosine and dopamine administration is almost unknown. This study aims to investigate the ventilatory response to ischemia and to adenosine, dopamine, and their antagonists in old rats, as well as the effect of hypoxia on adenosine 3′,5′-cyclic monophosphate (cAMP) accumulation in the aged CB. In vivo experiments were performed on young and aged rats anesthetized with pentobarbitone and breathing spontaneously. CB ischemia was induced AGE (2011) 33:337-350 DOI 10.1007 Scientific knowledge on the subject The functional ventilatory consequences of the morphological and molecular changes in the carotid body observed in aged animals, as well as the ventilatory effects of dopamine and adenosine in old animals, are still unknown.What this study adds to the field The carotid body's peripheral control of ventilation is not impaired by aging. The preservation of the inhibitory and excitatory effects on ventilation caused by exogenous dopamine and adenosine, respectively, should be taken into account in the therapeutic use of these amines and their agonists and antagonists in elderly people. by bilateral common carotid occlusions. cAMP content was measured in CB incubated with different oxygen concentrations. Hyperoxia caused a decrease in cAMP in the CB at all ages, but no differences were found between normoxia and hypoxia or between young and old animals. The endogenous dopaminergic inhibitory tonus is slightly reduced. However, both the ventilation decrease caused by exogenous dopamine and the increase mediated by A 2A -adenosine receptors are not impaired in aged animals. The bradycardia induced by adenosine is attenuated in old rats. The CB's peripheral control of ventilation is preserved during aging. Concerns have also arisen regarding the clinical usage of adenosine to revert supraventricular tachycardia and the use of dopamine in critical care situations involving elderly people.

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Section: Discussionsupporting

confidence: 88%

Carotid body function in aged rats: responses to hypoxia, ischemia, dopamine, and adenosine

Monteiro

Batuca

Obeso

et al. 2010

AGE

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“…Our data could therefore support the contention of Chen et al (1997) that the elevation of cAMP during hypoxia is mediated by the release of endogenous adenosine. However, in another study, no effects of cAMP or PKA were observed on currents recorded from neonatal rat type I cells (Hatton & Peers, 1996) and these authors argued against a role for cyclic nucleotides in chemotransduction.…”

Section: Discussionsupporting

confidence: 87%

Presynaptic action of adenosine on a 4‐aminopyridine‐sensitive current in the rat carotid body

Vandier

Conway

Landauer

et al. 1999

The Journal of Physiology

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1. Plasma adenosine concentration increases during hypoxia to a level that excites carotid body chemoreceptors by an undetermined mechanism. We have examined this further by determining the electrophysiological responses to exogenous adenosine of sinus nerve chemoafferents in vitro and of whole-cell currents in isolated type I cells. 2. Steady-state, single-fibre chemoafferent discharge was increased approximately 5-fold above basal levels by 100 ìÒ adenosine. This adenosine-stimulated discharge was reversibly and increasingly reduced by methoxyverapamil (D600, 100 ìÒ), by application of nickel chloride (Ni¥, 2 mÒ) and by removal of extracellular Ca¥. These effects strongly suggest a presynaptic, excitatory action of adenosine on type I cells of the carotid body. 3. Adenosine decreased whole-cell outward currents at membrane potentials above -40 mV in isolated type I cells recorded during superfusion with bicarbonate-buffered saline solution at 34-36°C. This effect was reversible and concentration dependent with a maximal effect at 10 ìÒ. 4. The degree of current inhibition induced by 10 ìÒ adenosine was voltage independent (45•39 ± 2•55 % (mean ± s.e.m.) between −40 and +30 mV) and largely (•75%), but not entirely, Ca¥ independent. 4-Aminopyridine (4-AP, 5 mÒ) decreased the amplitude of the control outward current by 80•60 ± 3•67 % and abolished the effect of adenosine. 5. Adenosine was without effect upon currents near the resting membrane potential of approximately −55 mV and did not induce depolarization in current-clamp experiments. 6. We conclude that adenosine acts to inhibit a 4-AP-sensitive current in isolated type I cells of the rat carotid body and suggest that this mechanism contributes to the chemoexcitatory effect of adenosine in the whole carotid body.

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“…Further to this, CO 2 is known to regulate cAMP concentrations in the carotid body, a peripheral chemosensor, independent of pH (54). Although a role for sAC versus G-protein-regulated ACs in this tissue remains to be investigated, the clear role for adenosine-mediated cAMP production in the carotid body is supportive of the latter (55).…”

Section: Resultsmentioning

confidence: 98%

Stimulation of Mammalian G-protein-responsive Adenylyl Cyclases by Carbon Dioxide

Townsend

Holliday

Fenyk

et al. 2009

Journal of Biological Chemistry

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Carbon dioxide is fundamental to the physiology of all organisms. There is considerable interest in the precise molecular mechanisms that organisms use to directly sense CO 2 . Here we demonstrate that a mammalian recombinant G-protein-activated adenylyl cyclase and the related Rv1625c adenylyl cyclase of Mycobacterium tuberculosis are specifically stimulated by CO 2 . Stimulation occurred at physiological concentrations of CO 2 through increased k cat . CO 2 increased the affinity of enzyme for metal co-factor, but contact with metal was not necessary as CO 2 interacted directly with apoenzyme. CO 2 stimulated the activity of both G-protein-regulated adenylyl cyclases and Rv1625c in vivo. Activation of G-protein regulated adenylyl cyclases by CO 2 gave a corresponding increase in cAMP-response element-binding protein (CREB) phosphorylation. Comparison of the responses of the G-protein regulated adenylyl cyclases and the molecularly, and biochemically distinct mammalian soluble adenylyl cyclase revealed that whereas G-protein-regulated enzymes are responsive to CO 2 , the soluble adenylyl cyclase is responsive to both CO 2 and bicarbonate ion. We have, thus, identified a signaling enzyme by which eukaryotes can directly detect and respond to fluctuating CO 2 .

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cAMP production in rabbit carotid body: role of adenosine

Cited by 25 publications

References 28 publications

Carotid body function in aged rats: responses to hypoxia, ischemia, dopamine, and adenosine

Carotid body function in aged rats: responses to hypoxia, ischemia, dopamine, and adenosine

Presynaptic action of adenosine on a 4‐aminopyridine‐sensitive current in the rat carotid body

Stimulation of Mammalian G-protein-responsive Adenylyl Cyclases by Carbon Dioxide

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