Acute withdrawal induced by adenosine A1-receptor activation in isolated guinea-pig ileum: role of opioid receptors and effect of cholecystokinin

2010 ◽  
Vol 62 (5) ◽  
pp. 622-632 ◽  
Author(s):  
Pietro Marini ◽  
Luca Romanelli ◽  
Daniela Valeri ◽  
Paolo Tucci ◽  
Pacifico Valeri ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Opioid Receptors ◽  
Receptor Activation ◽  
Adenosine A1 Receptor ◽  
Guinea Pig Ileum ◽  
Acute Withdrawal ◽  
Adenosine A1 ◽  
A1 Receptor

Immunohistochemical analysis on the role of the adenosine A1 receptor in epilepsy

1998 ◽  
Vol 31 ◽  
pp. S92
Author(s):  
Tomoyo Ochiishi ◽  
Masatoshi Takita ◽  
Shinya S. Suzuki ◽  
Mitsushi Ikemoto ◽  
Hiroyasu Nakata
Keyword(s):  
Immunohistochemical Analysis ◽  
Adenosine A1 Receptor ◽  
Adenosine A1 ◽  
A1 Receptor

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.

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