Effects of hypoxia and putative transmitters on [Ca 2+] i of rat glomus cells

• Published in: Brain research 2004-01, Vol.995 (2), p.285-296
• Main Authors: Jiang, R.G, Eyzaguirre, C
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Calcium - analysis; Cardiorespiratory control. Arterial mecano- and chemoreceptor; Carotid body; Carotid Body - cytology; Carotid Body - metabolism; Cells, Cultured; Chelating Agents; Dithionite - pharmacology; Fundamental and applied biological sciences. Psychology; Glomus cell; Hypoxia; Hypoxia - chemically induced; Hypoxia - metabolism; Intracellular calcium; Intracellular Fluid - chemistry; Intracellular Fluid - drug effects; Neurotransmitter Agents - pharmacology; Nitrogen - pharmacology; Rats; Rats, Wistar; Synaptic blocker; Transmitter; Vertebrates: respiratory system
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2003.09.075

Dissociated rat glomus cells were loaded with Fura-2 AM to study the effects of hypoxia, and carotid body transmitters on intracellular calcium, [Ca 2+] i. The mean control [Ca 2+] i was 55 nM in isolated cells and 67 nM in clusters. The following procedures changed [Ca 2+] i: (1) 0[Ca 2+] o+EGTA reduced [Ca 2+] i by about 50%, suggesting that the remaining calcium originated from intracellular organelles. [Ca 2+] i increased when [Ca 2+] o was doubled. (2) Hypoxia by sodium dithionite (Na 2S 2O 4) induced large [Ca 2+] i increases in clustered and isolated cells. Smaller rises occurred with 100% N 2 hypoxia. The augmented [Ca 2+] i, induced by Na 2S 2O 4, was reduced (not eliminated) in 0[Ca 2+] o+EGTA, suggesting that some calcium was intracellularly released. Nifedipine depressed (did not block) the Na 2S 2O 4-induced calcium increase, implying some inflow via other (N, T or P/Q) voltage-dependent or voltage-independent calcium channels. (3) Cholinergic agents (ACh, nicotine, muscarine, bethanechol and pilocarpine) increased [Ca 2+] i. The ACh effect was produced exclusively by calcium inflow since it was eliminated in 0[Ca 2+] o+EGTA. Cholinergic effects were depressed (not obliterated) by d-tubocurarine ( d-TC), hexamethonium (C6) and atropine. (4) ACh, nicotine and pilocarpine potentiated the excitatory effect of Na 2S 2O 4 on [Ca 2+] i. Bethanechol depressed this excitation whereas muscarine had inconsistent effects. (5) Atropine and C6 depressed [Ca 2+] i increases elicited by Na 2S 2O 4 but the effects of d-TC were variable. (6) Dopamine (DA) had variable effects. It increased [Ca 2+] i in 75% of cases, and reduced the Na 2S 2O 4 -induced calcium increase. Thus, calcium increases during Na 2S 2O 4 occur by direct effects on the glomus cells and feedback action through released ACh and DA.