Moderate cerebral venous congestion induces rapid cerebral protection via adenosine A1 receptor activation

2006 ◽  
Vol 1122 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Keiichi Akaiwa ◽  
Hidetoshi Akashi ◽  
Hideki Harada ◽  
Hideki Sakashita ◽  
Shinichi Hiromatsu ◽  
...  
Keyword(s):  
Receptor Activation ◽  
Cerebral Protection ◽  
Venous Congestion ◽  
Adenosine A1 Receptor ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Cerebral Venous Congestion

Regulation of Na(+)-3HCO3- cotransport in rabbit proximal convoluted tubule via adenosine A1 receptor

1993 ◽  
Vol 265 (4) ◽  
pp. F511-F519 ◽  
Author(s):  
M. Takeda ◽  
K. Yoshitomi ◽  
M. Imai
Keyword(s):  
Basolateral Membrane ◽  
Receptor Activation ◽  
Proximal Convoluted Tubule ◽  
Adenosine A1 Receptor ◽  
Intracellular Camp ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Adenosine A1 ◽  
A1 Receptor

We investigated the role of adenosine A1-receptor in the regulation of basolateral Na(+)-3HCO3- cotransporter in the rabbit proximal convoluted tubule (PCT) microperfused in vitro by monitoring basolateral membrane potential and intracellular pH. FK-453, a highly specific A1 antagonist, inhibited basolateral HCO3- conductance in a concentration-dependent manner (10(-10)-10(-5) M). Other A1 antagonists, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) at 10(-5) M and theophylline at 10(-3) M, also had similar effects. N6-cyclohexyladenosine (CHA) at 10(-7) M attenuated the effect of low concentration (10(-8) M) of FK-453. Either enhancement of the degradation of adenosine by 0.1 U/ml adenosine deaminase (ADA) or inhibition of adenosine release from the cells by 10(-6) M S-(4-nitrobenzyl)-6-thioinosine (NBTI) mimicked the effects of A1 antagonists. These observations suggest that endogenous adenosine is released from PCT cells and stimulates Na(+)-3HCO3- cotransporter. Both 10(-4) M 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate (CPT-cAMP) and 10(-6) M forskolin also inhibited basolateral HCO3- conductance. Both 10(-6) M FK-453 and 10(-4) M CPT-cAMP decreased the initial rate as well as the magnitude of intracellular acidification induced by reduction of peritubular HCO3- concentration from 25 to 0 mM. Neither 10(-6) M FK-453 nor 10(-7) M CHA changed intracellular Ca2+ concentration as measured by fura-2 fluorescence. These results indicate that adenosine might stimulate HCO3- exit across the basolateral membrane through Na(+)-3HCO3- cotransporter by decreasing intracellular cAMP via A1-receptor activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Modulation of ATP-sensitive K+ channels in rabbit ventricular myocytes by adenosine A1 receptor activation

1997 ◽  
Vol 272 (1) ◽  
pp. H325-H333 ◽  
Author(s):  
E. Kim ◽  
J. Han ◽  
W. Ho ◽  
Y. E. Earm
Keyword(s):  
Katp Channel ◽  
Ventricular Myocytes ◽  
Receptor Activation ◽  
Adenosine A1 Receptor ◽  
Channel Activity ◽  
Patch Clamp Technique ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Channel Analysis ◽  
Rabbit Ventricular Myocytes

The objective of the present study was to characterize the role of adenosine in the regulation of ATP-sensitive K (KATP) channel activity in isolated rabbit ventricular myocytes using the patch-clamp technique. In an outside-out patch exposed to guanosine 5'-triphosphate and ATP at the intracellular surface, external adenosine stimulated KATP channel activity. In an inside-out patch exposed to external adenosine, ATP reduced KATP channel activity and guanosine 5'-triphosphate stimulated KATP channel activity. Guanosine 5'-O-(3-thiotriphosphate) resulted in a gradual increase of KATP channel activity even in the absence of adenosine. When myocytes were preincubated with pertussis toxin or 8-cyclopentyl-1,3-dipropylxanthine, adenosine A1 receptor activation failed to activate the KATP channel. Analysis of the open and closed time distributions showed that adenosine A1 receptor activation increased burst duration and decreased interburst duration. In a dose-response relationship for ATP, adenosine A1 receptor activation shifted the half-maximal inhibition of the KATP channel from 70 to 241 microM.

scholarly journals Influence of β-adrenoceptor tone on the cardioprotective efficacy of adenosine A1 receptor activation in isolated working rat hearts

2000 ◽  
Vol 131 (3) ◽  
pp. 537-545 ◽  
Author(s):  
William R Ford ◽  
Bodh I Jugdutt ◽  
Gary D Lopaschuk ◽  
Rick Schulz ◽  
Alexander S Clanachan
Keyword(s):  
Receptor Activation ◽  
Adenosine A1 Receptor ◽  
Rat Hearts ◽  
Adenosine A1 ◽  
A1 Receptor

Adenosine attenuates calcium paradox injury: role of adenosine A1 receptor

1995 ◽  
Vol 268 (4) ◽  
pp. C838-C845 ◽  
Author(s):  
J. Suleiman ◽  
M. Ashraf
Keyword(s):  
Pertussis Toxin ◽  
Receptor Activation ◽  
Isolated Rat Heart ◽  
Adenosine A1 Receptor ◽  
Mechanical Activity ◽  
Dependent Manner ◽  
Protective Effects ◽  
Lactate Dehydrogenase Release ◽  
Adenosine A1 ◽  
A1 Receptor

The present study was conducted to test the hypothesis that adenosine attenuates the Ca2+ paradox (PD) injury via stimulation of adenosine A1 receptors linked to Gi proteins in the isolated rat heart. Treatment of adenosine reduced maximum lactate dehydrogenase release and ATP loss compared with regular Ca2+ PD. Recovery of mechanical activity after Ca2+ repletion was observed only in heart treated with adenosine before and during the Ca2+ PD. Significant preservation of myocytes was observed in adenosine-treated hearts compared with the regular Ca2+ PD. Adenosine exerted its effects in a dose-dependent manner, being maximum at 100 microM. The protective effects were mediated by adenosine A1 receptor activation since the adenosine A1 receptor agonist N6-phenylisopropyladenosine provided protection similar to adenosine-treated heart and was blocked by A1 receptor antagonist and pertussis toxin. This study suggests that protection by adenosine against the lethal injury of the Ca2+ PD is mediated by adenosine A1 receptor and a pertussis toxin-sensitive inhibiting G protein.

Adenosine A1 receptor activation modulates N-methyl-d-aspartate (NMDA) preconditioning phenotype in the brain

2015 ◽  
Vol 282 ◽  
pp. 103-110 ◽  
Author(s):  
Leandra C. Constantino ◽  
Fabrício A. Pamplona ◽  
Filipe C. Matheus ◽  
Fabiana K. Ludka ◽  
Maricel Gomez-Soler ◽  
...  
Keyword(s):  
Receptor Activation ◽  
Adenosine A1 Receptor ◽  
Nmda Preconditioning ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
The Brain
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