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We investigated the electrophysiological effects of cardiac hypertrophy induced by different experimental models. Comparison of the action potentials of hypertrophied and control rat hearts reveals a pronounced prolongation of the action potential fo

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Close examination of the effect of DPCPX alone showed an increase in forskolin-stimulated [3H]cAMP accumulation. This could have been secondary to DPCPX acting as either an A1-Gi-inverse agonist or a weak A1-Gs-agonist. An alternative explanation could be antagonism of secreted endogenous adenosine from the cells themselves. Concentration-response curves were therefore constructed to the antagonists alone. An augmentation of forskolin-stimulated [3H]cAMP accumulation was observed in response to all four antagonists. Furthermore, the log EC50 values of the antagonists for this response were very similar to the log KD values obtained from whole-cell binding. Closer examination of the responses to DPCPX and CGS 15943 indicated that the response curves were biphasic. When the responses were examined in the parent CHO-CRE-SPAP cells (i.e., those with the CRE-SPAP reporter but without the A1-receptor), a similar decrease in [3H]cAMP was seen at matching higher concentrations. This suggests that the ...

SCH 442416 is a selective adenosine A2A receptor antagonist; binds to human and rat A2A receptors with high affinity (Ki values are 0.048 and 0.5 nM respectively). Displays > 23000-fold selectivity for hA2A over hA1 in vitro with minimal affinity for h

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Hospitalization for acute heart failure (AHF) is a major public health problem, with ,1 million hospitalizations annually in the United States.1 The development of new therapies for patients with AHF remains a significant challenge.2 One aspect of clinical trial design in AHF that has been particularly vexing is the choice of appropriate end points, a topic that has recently been reviewed in detail.3 The lack of consensus on the best end points for AHF studies has led to a heterogeneous variety of end points in phase III studies, a disparity that limits the ability to make comparisons across studies.4. A notable feature of previous drug development programs in AHF has been the discrepancy between positive signals for efficacy in phase II studies and the lack of efficacy in more definitively powered phase III trials. This disconnect between phase II and phase III trials has now been observed with a variety of agents, including tezosentan,5 tolvaptan,6 and rolofylline.7 A notable paradox in ...

Merck has said that the preliminary results for its pivotal Phase III study of rolofylline (MK-7418), its investigational medicine for the treatment of acute heart failure, did not meet the primary or secondary efficacy endpoints in patients with heart failure.

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We examined how the endogenous anticonvulsant adenosine might influence gamma-aminobutyric acid type A (GABA(A)) receptor stability and which adenosine receptors (ARs) were involved. Upon repetitive activation (GABA 500 microM), GABA(A) receptors, microtransplanted into Xenopus oocytes from neurosurgically resected epileptic human nervous tissues, exhibited an obvious GABA(A)-current (I(GABA)) run-down, which was consistently and significantly reduced by treatment with the nonselective adenosine receptor antagonist CGS15943 (100 nM) or with adenosine deaminase (ADA) (1 units/ml), that inactivates adenosine. It was also found that selective antagonists of A2B (MRS1706, 10 nM) or A3 (MRS1334, 30 nM) receptors reduced I(GABA) run-down, whereas treatment with the specific A1 receptor antagonist DPCPX (10 nM) was ineffective. The selective A2A receptor antagonist SCH58261 (10 nM) reduced or potentiated I(GABA) run-down in approximately 40% and approximately 20% of tested oocytes, respectively. The ...

A method of treating cells having a reduced apical Cl.sup.- conductance, such as that characteristic of cystic fibrosis cells, by contacting cells having a reduced apical Cl.sup.- conductance with a therapeutically effective quantity of a compound that antagonizes the A.sub.1 -adenosine cell receptor and does not antagonize the A.sub.2 -adenosine cell receptor. Suitable compounds include 8-cyclopentyl-1,3-dipropylxanthine (CPX), xanthine amino congener (XAC), and therapeutically effective derivatives thereof.. ...

Action adenosinergic funds due to a direct interaction with adenozinovymi (purine) receptors and indirect effect on the disintegration and accumulation of adenosine (one of the purine neuromodulators). Specialized purine receptors (post - and presynaptic), divided into the P1 receptors (highly sensitive to adenosine) and P2 receptors (more sensitive to ATP). Both types are found in the Central nervous system, cardiovascular and respiratory system, lymph and platelets, etc.. It is known that adenosine has mainly cardiovascular effects, manifested by vasodilatation (with improvement of microcirculation and reduction of platelet aggregation) and negative Ino-, Chrono and dromotropony effects on the heart associated with inhibition of intracellular transport of calcium ions. A number of drugs (dipyridamole, papaverine, etc.) affect the metabolism of adenosine, contribute to its accumulation in the myocardium or potentiate the effect; used as koronarolitikov the disease ...

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Sweeney-Nixon, M. I., White, T., & Sawynok, J. (1989). Adenosine release from the spinal cord may mediate antinodideption by intracerebroventricular morphine. Society For Neuroscience Abstracts, 15, 371 ...

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TY - JOUR. T1 - Chronic caffeine exposure in rats blocks a subsequent nicotine-conditioned taste avoidance in a one-bottle, but not a two-bottle test. AU - Palmatier, Matthew I.. AU - Bevins, Rick A. PY - 2001/11/21. Y1 - 2001/11/21. N2 - Two experiments were conducted in order to investigate nicotine-conditioned taste avoidance (CTA) following chronic preexposure to caffeine. Rats were given daily intraperitoneal injections of caffeine anhydrous (0, 10, or 30 mg/kg) for 10 or 30 days. Training of the nicotine-CTA began after the last day of caffeine preexposure. On five separate occasions access to a saccharin solution was followed immediately by an injection of 1.2 mg/kg nicotine hydrogen tartrate salt or saline. Nicotine-CTA readily developed in saline-preexposed controls. That is, paired rats drank less saccharin solution than unpaired rats after repeated saccharin-nicotine pairings. A similar pattern of nicotine-CTA was found for rats preexposed to 30 mg/kg caffeine for 10 days. Following ...

August 20, 2007 By Grendel Burrell, M.D. [1] Preliminary results of the Phase 2, 50-patient, of BG9928 (ADENTRI®), an A1 adenosine receptor antagonist in stable patients with heart failure were reported in 2003 at the American Heart Associations annual scientific session. Dr. Barry Greenberg, professor of medicine and director of the Advanced Heart Failure Program at University of California, San Diego Medical Center, and colleagues reported the results in the August 14, 2007, issue of the Journal of the American College of Cardiology, in an article titled Effects of Multiple Oral Doses of an A1 Adenosine Antagonist, BG9928, in Patients With Heart Failure: Results of a Placebo-Controlled, Dose-Escalation Study (J Am Coll Cardiol, 2007; 50:600-606, doi:10.1016/j.jacc.2007.03.059 (Published online 29 July 2007)). BG9928 is a selective inhibitor of the A1 adenosine receptor. The objective of the study was to assess the pharmacokinetics and pharmacologic effects of BG9928 (ADENTRI®) in heart ...

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BioAssay record AID 602758 submitted by ChEMBL: Displacement of [3H]DPCPX from human recombinant adenosine A1 receptor expressed in CHO cell membranes by scintillation counting.

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