|1.||Nastasi, Giancarlo: 1 article (10/2013)|
|2.||Prestipino, Vera: 1 article (10/2013)|
|3.||Puzzolo, Domenico: 1 article (10/2013)|
|4.||D'Ascola, Angela: 1 article (10/2013)|
|5.||Campo, Giuseppe M: 1 article (10/2013)|
|6.||Scuruchi, Michele: 1 article (10/2013)|
|7.||Campo, Salvatore: 1 article (10/2013)|
|8.||Avenoso, Angela: 1 article (10/2013)|
|9.||Micali, Antonio: 1 article (10/2013)|
|10.||Pisani, Antonina: 1 article (10/2013)|
|1.||Hypotension (Low Blood Pressure)
11/01/1981 - "A moderate hypotension was induced by CV-1808, nifedipine, and nitroglycerin, while a significant reduction in cardiac function was seen after dosing with propranolol."
09/01/1990 - "Whereas a significant increase in renin release was evident in animals treated with CV-1808 and hydralazine, no change occurred in response to the NECA-, 2-CADO- or CPA-induced hypotension. "
12/01/1989 - "In contrast, heroic doses of the A2 selective ligand, 2-phenylaminoadenosine, afforded no protection against seizures. "
12/01/1989 - "The rank order of potency of these compounds in suppressing seizures is as follows: NECA greater than cyclohexyladenosine greater than cyclopentyladenosine greater than or equal to R-PIA greater than 2-chloroadenosine greater than S-PIA much greater than 2-phenylaminoadenosine. "
03/01/1997 - "The putative A4 agonist 2-phenylaminoadenosine (CV-1808; Cornfield et al., 1992) did not potentiate I(Ca) at four concentrations tested between 25 nM and 2500 nM. K0.5 for the APNEA-induced potentiation was 25.4 nM, comparable to that determined in binding studies for the cloned receptor (15.5 nM; Zhou et al., 1992). "
01/01/1996 - "2. The rank order of agonist potency in inducing decreases in diastolic blood pressure was N6-cyclopentyladenosine (CPA) > N6-cyclohexyladenosine (CHA) > N-ethyl-carboxamidoadenosine (NECA) > or = 2-phenylaminoadenosine (CV1808) > 2-p-(carboxyethyl)phenethylamino-5' N-ethylcarboxamidoadenosine (CGS 21680) > N6-(2-(4-aminophenyl)ethyl)-adenosine (APNEA). "
11/01/1994 - "The compounds tested were: the A1/A3 receptor agonist, N-[2-(4-aminophenyl)ethyl]adenosine (APNEA), the non-selective adenosine receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA), the adenosine A1 receptor-selective agonists, N-[(1S,trans)-2-hydroxycyclopentyl]adenosine (GR79236) and N6-cyclopentyl adenosine (CPA), the A2a receptor-selective agonists, 2-[[2-[4-(2-carboxyethyl) phenyl] ethyl] amino]-N- ethylcarboxamidoadenosine (CGS21680) and 2-phenylaminoadenosine (CV1808), and the moderately A2b selective agonist, N-[(2-methylphenyl)methyl]adenosine (metrifudil). "
11/01/1981 - "In hearts with continuous coronary occlusion, CV-1808 (0.3 and 1.0 microgram/kg, i.v. bolus) increased the retrograde blood flow from the ischemic area immediately after administration, suggesting a collateral vasodilating action. "
05/01/1984 - "CV-1808 (0.25 microgram/kg/min i.v. infusion throughout the experimental period, starting 10 min before coronary occlusion) inhibited coronary circulatory failure and TXA2 release. "
05/01/1984 - "Inhibition of coronary circulatory failure and thromboxane A2 release during coronary occlusion and reperfusion by 2-phenylaminoadenosine (CV-1808) in anesthetized dogs."
01/01/1990 - "2-Phenylaminoadenosine hyperalgesia is prolonged by rolipram, a phosphodiesterase inhibitor. "
01/01/1990 - "Both 2-phenylaminoadenosine and prostaglandin E2 hyperalgesia are antagonized by the A1-agonist N6-cyclopentyladenosine and the mu-agonist, [D-Ala2, NMe-Phe4, Gly-ol]enkephalin. "
01/01/1990 - "The latency to onset of adenosine and 2-phenylaminoadenosine hyperalgesia is similar to that produced by prostaglandin E2, a directly acting hyperalgesic agent but shorter than that produced by leukotriene B4, which acts indirectly. "
01/01/1990 - "Adenosine-induced hyperalgesia is mimicked by the A2-agonists, 5'-(N-ethyl)-carboxamido-adenosine and 2-phenylaminoadenosine but not by the A1-agonist, N6-cyclopentyladenosine and antagonized by the adenosine A2-receptor antagonist, PD 081360-0002 but not by the A1-antagonist, 1,3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine. "
01/01/1991 - "The Rp isomer of cyclic adenosine-3'5'-monophosphothioate also inhibited the hyperalgesia induced by a membrane-permeable analogue of cAMP, 8-bromocyclic adenosine monophosphate, as well as the hyperalgesia induced by agents that are presumed to act directly on primary afferent nociceptors: prostaglandin E2, prostaglandin I2, (8R,15S)-dihydroxyicosa(5E-9,11,13Z)tetraenoic acid; and the adenosine A2-agonist 2-phenylaminoadenosine. "
|7.||Purinergic P1 Receptors (Adenosine Receptor)