Analgesic effect of paeoniflorin in rats with neonatal maternal separation-induced visceral hyperalgesia is mediated through adenosine A1 receptor by inhibiting the extracellular signal-regulated protein kinase (ERK) pathway

2009 ◽  
Vol 94 (1) ◽  
pp. 88-97 ◽  
Author(s):  
Xiao-Jun Zhang ◽  
Hong-Li Chen ◽  
Zhi Li ◽  
Hong-Qi Zhang ◽  
Hong-Xi Xu ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Analgesic Effect ◽  
Maternal Separation ◽  
Adenosine A1 Receptor ◽  
Erk Pathway ◽  
Visceral Hyperalgesia ◽  
Extracellular Signal ◽  
Adenosine A1 ◽  
Neonatal Maternal Separation ◽  
A1 Receptor

Upregulated renal adenosine A1 receptors augment PKC and glucose transport but inhibit proliferation

1996 ◽  
Vol 270 (2) ◽  
pp. F263-F274 ◽  
Author(s):  
R. Coulson ◽  
P. S. Proch ◽  
R. A. Olsson ◽  
C. E. Chalfant ◽  
D. R. Cooper
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Adenosine Receptor ◽  
Adenosine A1 Receptor ◽  
Receptor Antagonists ◽  
Caffeine Treatment ◽  
Adenosine A1 ◽  
A1 Receptor

Adenosine A1 receptor densities were increased in cultured LLC-PK1 and OK cells by chronic treatment with the adenosine receptor antagonists 1,3,7-trimethylxanthine (caffeine, 1 mM) and 1,3-dimethyl-8-cyclopentylxanthine [cyclopentyltheophylline (CPT), < or = 0.4 mM], respectively. The A1 receptor number per cell was increased twofold by 10-day treatments with 1 mM caffeine or 0.1 mM CPT, and the sodium-coupled glucose uptake was augmented twofold by 1 mM caffeine and sevenfold by 0.1 microM CPT (higher doses of CPT were progressively less stimulatory). Glucose uptake was blocked by acute (2-h) treatment with CPT, adenosine deaminase, or calphostin C. Caffeine (1 mM) or CPT (> or = 0.1 mM) inhibited cell proliferation for the first 10 days, then cell growth assumed a normal proliferative rate despite continued presence of antagonist. Cytosolic protein kinase C (PKC) beta-isoform immunoactivity and PKC-beta II mRNA were elevated at least twofold during 10 days of 0.1 mM CPT or 1 mM caffeine treatment. The sustained elevation in sodium-glucose symport and PKC activity observed with adenosine receptor antagonists was similar to acute (2-h) effects of the adenosine A1 agonist R(-)-N6-phenylisopropyladenosine (R-PIA, 0.1-1 microM). Moreover, cell proliferation was increased by adenosine (0.1 microM R-PIA), whereas Na-K-adenosinetriphosphatase activity was unaltered with chronic antagonist or acute adenosine treatments. Caffeine treatment may have some non-adenosine A1 receptor-mediated actions, because it slightly (30%) augmented protein kinase A activity. It is concluded that chronic exposure of proximal tubule cells to caffeine or CPT augments PKC and sodium-glucose transport but retards cell proliferation mainly via adenosine A1 receptor-mediated mechanisms.

scholarly journals A role of protein kinase Cμ in signalling from the human adenosine A1 receptor to the nucleus

2003 ◽  
Vol 139 (4) ◽  
pp. 721-732 ◽  
Author(s):  
Kathryn J Hill ◽  
Anne C Webber ◽  
Stephen J Hill
Keyword(s):  
Protein Kinase ◽  
Adenosine A1 Receptor ◽  
Adenosine A1 ◽  
A1 Receptor

scholarly journals Effects of adenosine A1 receptor antagonism on lipogenesis and lipolysis in isolated rat adipocytes

2009 ◽  
pp. 863-871
Author(s):  
T Szkudelski ◽  
K Szkudelska ◽  
L Nogowski
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Synergistic Action ◽  
Adenosine A1 Receptor ◽  
Weak Effect ◽  
Rat Adipocytes ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Release Of Glycerol ◽  
Kinase A

Adenosine is secreted from adipocytes, binds to adenosine A1 receptor and modulates various functions of these cells. In the present study, the effects of an adenosine A1 receptor antagonist (DPCPX; 0.01, 0.1 and 1 μM) on lipogenesis, glucose transport, lipolysis and the antilipolytic action of insulin were tested in rat adipocytes. DPCPX had a very weak effect on lipogenesis and did not significantly affect glucose uptake. In adipocytes incubated with 1 μM DPCPX, lipolysis increased. This effect was blunted by insulin and by a direct inhibitor of protein kinase A. Moreover, 0.1 μM DPCPX substantially enhanced the lipolytic response to epinephrine and increased cAMP in adipocytes. However, DPCPX was ineffective when lipolysis was stimulated by direct activation of protein kinase A. Adipocyte exposure to epinephrine and insulin with or without 0.1 μM DPCPX demonstrated that this antagonist increased the release of glycerol. However, despite the presence of DPCPX, insulin was able to reduce lipolysis. It is concluded that DPCPX had a weak effect on lipogenesis, whereas lipolysis was significantly affected. The partial antagonism of adenosine A1 receptor increased lipolysis in cells incubated with epinephrine alone and epinephrine with insulin due to the synergistic action of 0.1 μM DPCPX and epinephrine.

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