Effects of a Dopamine Agonist on Cytosolic Ca2+ Changes Induced by Hypoxia in Rat Glomus Cells

Yoshizaki, Kazuhito; Momiyama, Hideki; Hayashida, Yoshiaki

doi:10.1007/0-306-46825-5_74

Cited by 4 publications

(1 citation statement)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inhibitory effects of dopamine on cat and rabbit carotid body chemosensory responses have also been observed as reviewed recently (Iturriaga and Alcayaga, 2004; Nurse and Piskuric, 2013). In rat glomus cells, dopamine (100 µM) inhibited Na 2 S 2 O 4 -induced increase in [Ca 2+ ] i in a small fraction of cells (Jiang and Eyzaguirre, 2004), and tyramine, used as a dopamine agonist, showed little or no effect on hypoxia-induced changes in [Ca 2+ ] i (Yoshizaki et al, 2000). These studies in rat glomus cells do not directly test the effect of dopamine itself on hypoxia-induced changes in [Ca 2+ ] i .…”

Section: Discussionmentioning

confidence: 99%

Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells

Wang

Hogan

Kim

2017

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

Recent study showed that hypoxia activates a Ca2+-sensitive, Na+-permeable non-selective cation channel (NSC) in carotid body glomus cells. We studied the effects of mitochondrial inhibitors that increase Ca2+ influx via Ca2+ channel (Cav), and receptor agonists that release Ca2+ from endoplasmic reticulum (ER) on NSC. Mitochondrial inhibitors (NaCN, FCCP, H2S, NO) elevated [Ca2+]i and activated NSC. Angiotensin II and acetylcholine that elevate [Ca2+]i via the Gq-IP3 pathway activated NSC. However, endothelin-1 (Gq) and 5-HT (Gq) showed little or no effect on [Ca2+]i and did not activate NSC. Adenosine (Gs) caused a weak rise in [Ca2+]i but did not activate NSC. Dopamine (Gs) and γ-aminobytyric acid (Gi) were ineffective in raising [Ca2+]i and failed to activate NSC. Store-operated Ca2+ entry (SOCE) produced by depletion of Ca2+ stores with cyclopiazonic acid activated NSC. Our results show that Ca2+ entry via Cav, ER Ca2+ release and SOCE can activate NSC. Thus, NSC contributes to both voltage- and receptor-mediated excitation of glomus cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells

Wang

Hogan

Kim

2017

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

show abstract

Electrical properties of chemoreceptor elements in the carotid body

Hayashida¹,

Hirakawa²

2002

Microscopy Res & Technique

View full text Add to dashboard Cite

The electrical properties of chemoreceptor afferent nerve fibers and glomus cells and the behavior of cytosolic Ca(2+) in glomus cells are reviewed. While this has not been confirmed, spontaneously depolarizing potentials (SDPs) recorded in a chemoreceptor afferent terminal may be the postsynaptic expression of presynaptic events. Glomus cells, which are presynaptic elements, either depolarized or hyperpolarized in response to natural and chemical stimulation. After-hyperpolarization following an initial depolarization and after-depolarization following an initial hyperpolarization were often seen. When a glomus cell depolarizes, voltage noise increases despite a decrease in input resistance in both intact and denervated carotid bodies. The voltage noise may be "receptor noise" generated in the glomus cell itself. The electrical properties of glomus cells change in the denervated carotid body, which suggests that the chemoreceptor afferent nerve exerts some trophic effect(s) on glomus cells. Hypoxia either increases or decreases cytosolic Ca(2+), while ACh or NaCN induces either an increase or no change in cytosolic Ca(2+) in glomus cells. There are at least two possible explanations for voltage changes in glomus cells: a chemical stimulus first depolarizes the glomus cell and induces Ca(2+) influx to release chemical substances, or a chemical stimulus induces an increase in [Ca(2+)](i) and then hyperpolarizes the glomus cell via potassium influx.

show abstract

Effects of hypoxia and putative transmitters on [Ca2+]i of rat glomus cells

Jiang

Eyzaguirre

2004

Brain Research

View full text Add to dashboard Cite

Effects of a Dopamine Agonist on Cytosolic Ca2+ Changes Induced by Hypoxia in Rat Glomus Cells

Cited by 4 publications

References 11 publications

Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells

Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells

Electrical properties of chemoreceptor elements in the carotid body

Effects of hypoxia and putative transmitters on [Ca2+]i of rat glomus cells

Contact Info

Product

Resources

About