N(6)-cyclopentyladenosine

04/01/2005 - "[Therapeutic efficacy of N6-cyclopentyladenosine against acute dichlorvos poisoning]."
04/01/2005 - "To study the therapeutic efficacy and mechanism of adenosine receptor agonist N(6)-cyclopentyladenosine (CPA) against acute dichlorvos poisoning. "
01/01/2004 - "Cardiovascular effects of the adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) decisive for its therapeutic efficacy in sarin poisoning."
07/01/2006 - "Therapy with N(6)-cyclopentyladenosine (CPA), physostigmine, hyoscine and HI-6 protected guinea-pigs against the incapacitating and lethal effects of a supralethal challenge of soman (135 microg/kg) when given 1 min after poisoning. "

07/01/2003 - "Protective effects of anticovulsant agents, N6-cyclopentyladenosine (CPA) and flunarizine (FLN) against aminophylline (AMPH) (280 mg/kg)-induced convulsions were tested in different groups of mice. "
07/01/2003 - "Individual and combined effects of N6-cyclopentyladenosine, flunarizine and diazepam on aminophylline-induced recurrent generalized seizures in mice."
11/16/1993 - "The effect of the adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) and antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX) on N-methyl-D-aspartate (NMDA)-evoked seizures was studied in C57BL/6 mice (20/group). "
05/01/1999 - "Angiotensin II (ANG II), its peptide analogue sarmesin, the selective adenosine A1 receptor agonists N6-cyclopentyladenosine (CPA) and 2-chloroadenosine (2-ClAdo) significantly increased the PTZ seizure threshold. "
02/21/1994 - "The effect of chronic administration of the adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) and the adenosine A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX) on N-methyl-D-aspartate (NMDA)-evoked seizures was studied in C57BL/6 mice (20/group). "

11/30/1993 - "Pertussis toxin pretreatment essentially abolished the bradycardia induced by the prototype A1 receptor agonist, N6-cyclopentyladenosine, whereas the fall in blood pressure induced by the selective A2A receptor agonist, CGS 21680 was enhanced. "
06/01/1999 - "This improved side effect profile contrasts markedly with the profound hypotension, bradycardia, and hypothermia and greater inhibition of motor function observed with the adenosine receptor agonist N6-cyclopentyladenosine and opens the way to clinical evaluation of AK inhibitors as a novel, adenosine-based approach to anticonvulsant therapy."
02/01/1993 - "The cardiovascular effects of N6-cyclopentyladenosine (CPA), a selective adenosine A1 receptor agonist and 2-[p-carboxyethyl)phenylethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21,680), a selective A2 receptor agonist have been investigated in the pithed rat with blood pressure raised to normal levels with angiotensin II. Cumulative intravenous administration of CPA, 0.3-10 micrograms/kg, induced dose-related falls in blood pressure and heart rate; over the same dose range CGS 21,680 induced hypotension but no bradycardia. "

08/14/2013 - "We previously observed that the adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) is a very effective antinociceptive agent on intact but not on spinalized adult rats with inflammation. "
08/12/2005 - "The adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) is very effective in reducing wind-up in intact but not in spinalized adult rats with carrageenan-induced inflammation, suggesting an adenosine-mediated supraspinal modulation. "

07/01/1999 - "We conclude that: (1) effective mutual synchronization with minimal fluctuation happens within the sino-atrial node of intact rat hearts at body temperature, and synchronization is not affected even by extreme changes in pre- and afterload, (2) the sino-atrial node is the sole source of BI variability in the intact isolated rat heart, (3) low temperature hampers this functional organization which can be reestablished by sinus node accelerating agents (isoprenaline, theophylline), (4) decreasing frequency by N6-Cyclopentyladenosine at normothermia also increases BI variability but less pronouncedly than hypothermia does."
06/01/1999 - "This improved side effect profile contrasts markedly with the profound hypotension, bradycardia, and hypothermia and greater inhibition of motor function observed with the adenosine receptor agonist N6-cyclopentyladenosine and opens the way to clinical evaluation of AK inhibitors as a novel, adenosine-based approach to anticonvulsant therapy."