Nitric Oxide and Carotid Body Chemoreception: Multiple Target Sites

2003 ◽  
pp. 451-462
Keyword(s):  
Nitric Oxide ◽  
Carotid Body ◽  
Multiple Target ◽  
Target Sites

Nitric Oxide in Brain Glucose Retention after Carotid Body Receptors Stimulation with Cyanide in Rats

2006 ◽  
pp. 293-300 ◽  
Author(s):  
S.A. MONTERO ◽  
J.L. CADENAS ◽  
M. LEMUS ◽  
E. ROCES DE ÁLVAREZ-BUYLLA. ◽  
R. ÁLVAREZ-BUYLLA.
Keyword(s):  
Nitric Oxide ◽  
Carotid Body ◽  
Brain Glucose

scholarly journals Nitric Oxide Inhibits L-Type Ca2+ Current in Glomus Cells of the Rabbit Carotid Body Via a cGMP-Independent Mechanism

1999 ◽  
Vol 81 (4) ◽  
pp. 1449-1457 ◽  
Author(s):  
Beth A. Summers ◽  
Jeffrey L. Overholt ◽  
Nanduri R. Prabhakar
Keyword(s):  
Nitric Oxide ◽  
Carotid Body ◽  
Channel Blocker ◽  
Adult Rabbit ◽  
Subsequent Formation ◽  
No Donors ◽  
Glomus Cells ◽  
Channel Proteins ◽  
Carotid Bodies ◽  
Independent Mechanism

Nitric oxide inhibits L-type Ca2+ current in glomus cells of the rabbit carotid body via a cGMP-independent mechanism. Previous studies have shown that nitric oxide (NO) inhibits carotid body sensory activity. To begin to understand the cellular mechanisms associated with the actions of NO in the carotid body, we monitored the effects of NO donors on the macroscopic Ca2+ current in glomus cells isolated from rabbit carotid bodies. Experiments were performed on freshly dissociated glomus cells from adult rabbit carotid bodies using the whole cell configuration of the patch-clamp technique. The NO donors sodium nitroprusside (SNP; 600 μM, n = 7) and spermine nitric oxide (SNO; 100 μM, n = 7) inhibited the Ca2+ current in glomus cells in a voltage-independent manner. These effects of NO donors were rapid in onset and peaked within 1 or 2 min. In contrast, the outward K+ current was unaffected by SNP (600 μM, n = 6), indicating that the inhibition by SNP was not a nonspecific membrane effect. 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy-PTIO; 500 μM), an NO scavenger, prevented inhibition of the Ca2+ current by SNP ( n = 7), whereas neither superoxide dismutase (SOD; 2,000 U/ml, n = 4), a superoxide scavenger, nor sodium hydrosulfite (SHS; 1 mM, n = 7), a reducing agent, prevented inhibition of the Ca2+ current by SNP. However, SNP inhibition of the Ca2+ current was reversible in the presence of either SOD or SHS. These results suggest that NO itself inhibits Ca2+current in a reversible manner and that subsequent formation of peroxynitrites results in irreversible inhibition. SNP inhibition of the Ca2+ current was not affected by 30 μM LY 83,583 ( n = 7) nor was it mimicked by 600 μM 8-bromoguanosine 3′:5′-cyclic monophosphate (8-Br-cGMP; n = 6), suggesting that the effects of NO on the Ca2+ current are mediated, in part, via a cGMP-independent mechanism. N-ethylmaleimide (NEM; 2.5 mM, n= 6) prevented the inhibition of the Ca2+ current by SNP, indicating that SNP is acting via a modification of sulfhydryl groups on Ca2+ channel proteins. Norepinephrine (NE; 10 μM) further inhibited the Ca2+ current in the presence of NEM ( n = 7), implying that NEM did not nonspecifically eliminate Ca2+ current modulation. Nisoldipine, an L-type Ca2+ channel blocker (2 μM, n = 6), prevented the inhibition of Ca2+ current by SNP, whereas ω-conotoxin GVIA, an N-type Ca2+ channel blocker (1 μM, n = 9), did not prevent the inhibition of Ca2+ current by SNP. These results demonstrate that NO inhibits L-type Ca2+ channels in adult rabbit glomus cells, in part, due to a modification of calcium channel proteins. The inhibition might provide one plausible mechanism for efferent inhibition of carotid body activity by NO.

scholarly journals MucR binds multiple target sites in the promoter of its own gene and is a heat‐stable protein: Is MucR a H‐ NS ‐like protein?

FEBS Open Bio ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 711-718 ◽  
Author(s):  
Ilaria Baglivo ◽  
Luciano Pirone ◽  
Gaetano Malgieri ◽  
Roberto Fattorusso ◽  
Roy Martin Roop II ◽  
...  
Keyword(s):  
Multiple Target ◽  
Heat Stable ◽  
Target Sites ◽  
Heat Stable Protein

Does chronic hypoxia increase rat carotid body nitric oxide?

1998 ◽  
Vol 120 (2) ◽  
pp. 243-247 ◽  
Author(s):  
C. Di Giulio ◽  
A. Grilli ◽  
M.A. De Lutiis ◽  
F. Di Natale ◽  
G. Sabatino ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carotid Body ◽  
Chronic Hypoxia

scholarly journals Attenuated outward potassium currents in carotid body glomus cells of heart failure rabbit: involvement of nitric oxide

2004 ◽  
Vol 555 (1) ◽  
pp. 219-229 ◽  
Author(s):  
Yu-Long Li ◽  
Shu-Yu Sun ◽  
Jeffery L. Overholt ◽  
Nanduri R. Prabhakar ◽  
George J. Rozanski ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Carotid Body ◽  
Potassium Currents ◽  
Glomus Cells ◽  
Carotid Body Glomus Cells

Nitric oxide in the sensory function of the carotid body

1993 ◽  
Vol 625 (1) ◽  
pp. 16-22 ◽  
Author(s):  
Nanduri R. Prabhakar ◽  
Ganesh K. Kumar ◽  
Chang Ho Chang ◽  
Faton H. Agani ◽  
Musa A. Haxhiu
Keyword(s):  
Nitric Oxide ◽  
Carotid Body ◽  
Sensory Function

Expression of nitric oxide-containing structures in the rat carotid body

2016 ◽  
Vol 118 (8) ◽  
pp. 770-775 ◽  
Author(s):  
Dimitrinka Y. Atanasova ◽  
Nikolay D. Dimitrov ◽  
Nikolai E. Lazarov
Keyword(s):  
Nitric Oxide ◽  
Carotid Body
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