A Quantitative Immunocytochemical Approach to the Analysis of Type I Cells in the Cat Carotid Body

Major, Jennifer; Dinger, B.; Stensaas, L. J.; Wang, Zuo-Zhong

doi:10.1159/000014611

Cited by 2 publications

(3 citation statements)

References 16 publications

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“…Carotid bodies were stained for TH or CGA, established markers of glomus cells (9,10). Both TH and CGA yielded qualitatively similar results.…”

Section: Ros Mediates Ih-induced Augmented Hsr But Not the Mor-mentioning

confidence: 88%

“…Each level of hypoxia was maintained for 5 min followed by a recovery period of 5 min. In series 3, morphometric analysis of carotid bodies was performed on control, IH, and IH ϩ MnTMPyP treated rat pups (n ϭ 6 carotid bodies from 3 pups in each group) with two established markers of glomus cells: TH and CGA (9,10). In series 4, ET-1-like immunoreactivity in carotid body from control and IH-conditioned rat pups was determined (n ϭ 3 pups in each group).…”

Section: Methodsmentioning

confidence: 99%

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Reactive oxygen species-dependent endothelin signaling is required for augmented hypoxic sensory response of the neonatal carotid body by intermittent hypoxia

Pawar

Nanduri²,

Yuan³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

116

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We previously reported that intermittent hypoxia (IH) augments hypoxic sensory response (HSR) and increases the number of glomus cells in neonatal carotid bodies. In the present study, we tested the hypothesis that recruitment of endothelin-1 (ET-1) signaling by reactive oxygen species (ROS) plays a critical role in IH-evoked changes in neonatal carotid bodies. Experiments were performed on neonatal rats exposed either to 10 days of IH (P0-P10; 8 h/day) or to normoxia. IH augmented HSR of the carotid bodies ex vivo and resulted in hyperplasia of glomus cells. The effects of IH were associated with enhanced basal release of ET-1 under normoxia, sensitization of carotid body response to exogenous ET-1, and upregulation of ET(A) but not an ET(B) receptor mRNA without altering the ET-1 content. An ET(A) but not ET(B) receptor antagonist prevented augmented HSR by IH. ROS levels were elevated in carotid bodies from IH-treated rat pups as evidenced by increased levels of malondialdehyde. Systemic administration of manganese (III) tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (MnTMPyP; 5 mg/kg ip), a scavenger of O(2)(*-), prevented IH-induced elevation of ROS, basal release of ET-1, upregulation of ET(A) mRNA, and augmented HSR. In striking contrast, MnTMPyP treatment had no significant effect on IH-induced hyperplasia of glomus cells. These results demonstrate that IH-evoked increase in HSR involve a ROS-mediated increase in basal ET-1 release and upregulation of ET(A) receptor mRNA.

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“…Carotid bodies were stained for TH or CGA, established markers of glomus cells (9,10). Both TH and CGA yielded qualitatively similar results.…”

Section: Ros Mediates Ih-induced Augmented Hsr But Not the Mor-mentioning

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Reactive oxygen species-dependent endothelin signaling is required for augmented hypoxic sensory response of the neonatal carotid body by intermittent hypoxia

Pawar

Nanduri²,

Yuan³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

116

View full text Add to dashboard Cite

show abstract

“…1a). To further confirm that ACh-expressing cells were indeed glomus cells, cells were double stained with monoclonal antibody for TH, an established marker of glomus cells (32,38) (Fig. 1b) Values are means Ϯ SE; n ϭ no.…”

Section: Ach Content and Localization In The Rabbit Carotid Bodymentioning

confidence: 97%

Acetylcholine release from the carotid body by hypoxia: evidence for the involvement of autoinhibitory receptors

Kim

Prabhakar²,

Kumar³

2004

Journal of Applied Physiology

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The purpose of the present study was to investigate whether hypoxia influences acetylcholine (ACh) release from the rabbit carotid body and, if so, to determine the mechanism(s) associated with this response. ACh is expressed in the rabbit carotid body (5.6 +/- 1.3 pmol/carotid body) as evidenced by electrochemical analysis. Immunocytochemical analysis of the primary cultures of the carotid body with antibody specific to ACh further showed that ACh-like immunoreactivity is localized to many glomus cells. The effect of hypoxia on ACh release was examined in ex vivo carotid bodies harvested from anesthetized rabbits. The basal release of ACh during normoxia ( approximately 150 Torr) averaged 5.9 +/- 0.5 fmol.min-1.carotid body-1. Lowering the Po2 to 90 and 20 Torr progressively decreased ACh release by approximately 15 and approximately 68%, respectively. ACh release returned to the basal value on reoxygenation. Simultaneous monitoring of dopamine showed a sixfold increase in dopamine release during hypoxia. Hypercapnia (21% O2 + 10% CO2) as well as high K+ (100 mM) facilitated ACh release from the carotid body, suggesting that hypoxia-induced inhibition of ACh release is not due to deterioration of the carotid body. Hypoxia had no significant effect on acetylcholinesterase activity in the medium, implying that increased hydrolysis of ACh does not account for hypoxia-induced inhibition of ACh release. In the presence of either atropine (10 microM) or domperidone (10 microM), hypoxia stimulated ACh release. These results demonstrate that glomus cells of the rabbit carotid body express ACh and that hypoxia overall inhibits ACh release via activation of muscarinic and dopaminergic autoinhibitory receptors in the carotid body.

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A Quantitative Immunocytochemical Approach to the Analysis of Type I Cells in the Cat Carotid Body

Cited by 2 publications

References 16 publications

Reactive oxygen species-dependent endothelin signaling is required for augmented hypoxic sensory response of the neonatal carotid body by intermittent hypoxia

Reactive oxygen species-dependent endothelin signaling is required for augmented hypoxic sensory response of the neonatal carotid body by intermittent hypoxia

Acetylcholine release from the carotid body by hypoxia: evidence for the involvement of autoinhibitory receptors

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