Редактирование: ADO (раздел)

==Publications==

{{medline-entry
|title=Reduced adenosine release from the aged mammalian heart.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22378276
|abstract=Adenosine ([[ADO]]) released in the heart results in enhanced coronary blood flow and reduced catecholamine release and myocardial responsiveness to adrenergic stimulation (anti-adrenergic action). [[ADO]] release from the adrenergic-stimulated aged heart is less than that from the young adult heart. Because adrenergic signaling in the aged heart is impaired, this study was conducted to determine if reduced [[ADO]] release from the aged heart results from this reduced adrenergic responsiveness. Hearts of 3-4 months (young adult) and 21-22 months (aged) Fischer-344 rats were perfused with [[ADO]] deamination and re-phosphorylation inhibited. Coronary effluent [[ADO]] levels were determined. Cellular-free [[ADO]] levels with and without sodium acetate (NaAc)-induced mitochondrial AMP synthesis were assessed using formed S-adenosylhomocysteine (SAH) in L-homocysteine thiolactone (L-HC)-treated hearts. The activities of SAH-hydrolase were determined. Aged heart [[ADO]] release was 61% less than from young hearts. NaAc augmented young heart [[ADO]] release by 104%, while that of aged hearts remained unchanged. SAH synthesis was 51% and 56% lower in the aged heart in the absence and presence of NaAc, respectively, despite an 89% greater SAH hydrolase activity found in the aged hearts. Since synthesized AMP may be diverted to IMP and ultimately inosine by AMP deaminase, inosine release was determined. Aged heart inosine levels in the absence and presence of NaAc were 74% and 59% less than for the young hearts. It is concluded that a reduced mitochondrial AMP synthesis is in part responsible for the attenuation in [[ADO]] release from the adrenergic-stimulated aged heart.
|mesh-terms=* Adenine
* Adenosine
* Adenosine Deaminase
* Adenosine Deaminase Inhibitors
* Adrenergic Antagonists
* Aging
* Animals
* Heart
* Hydrolases
* Male
* Myocardial Contraction
* Perfusion
* Rats
* Rats, Inbred F344
* S-Adenosylhomocysteine
* Sodium Chloride
* Tubercidin

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384761
}}
{{medline-entry
|title=Adenosine A2A receptor modulation of juvenile female rat skeletal muscle microvessel permeability.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/16815983
|abstract=Little is known of the regulation of skeletal muscle microvascular exchange under resting or stimulating conditions. Adenosine ([[ADO]]) levels in skeletal muscle increase during physiological (exercise) and pathological (hypoxia, inflammation, and ischemia) conditions. Later stages of these pathologies are characterized by the loss of vascular barrier integrity. This study focused on determining which [[ADO]] receptor mediates the robust reduction in microvessel permeability to rat serum albumin (P(s)(RSA)) observed in juvenile female rats. In microvessels isolated from abdominal skeletal muscle, [[ADO]] suffusion induced a concentration-dependent reduction in arteriolar [log(IC(50)) = -9.8  /- 0.2 M] and venular [log(IC(50)) = -8.4  /- 0.2 M] P(s)(RSA). RT-PCR and immunoblot analysis demonstrated mRNA and protein expression of [[ADO]] A(1), A(2A), A(2B), and A(3) receptors in both vessel types, and immunofluorescence assay revealed expression of the four subtype receptors in the microvascular walls (endothelium and smooth muscle). P(s)(RSA) responses of arterioles and venules to [[ADO]] were blocked by 8-(p-sulphophenyl)theophylline, a nonselective A(1) and A(2) antagonist. An A(2A) agonist, CGS21680, was more potent than the A(1) agonist, cyclopentyladenosine, or the most-selective A(2B) agonist, 5'-(N-ethylcarboxamido)adenosine. The ability of CGS21680 or [[ADO]] to reduce P(s)(RSA) was abolished by the A(2A) antagonist, ZM241385. An adenylyl cyclase inhibitor, SQ22536, blocked the permeability response to [[ADO]]. In aggregate, these results demonstrate that, in juvenile females (before the production of the reproductive hormones), [[ADO]] enhances skeletal muscle arteriole and venule barrier function predominantly via A(2A) receptors using activation of adenylyl cyclase-signaling mechanisms.
|mesh-terms=* Adenine
* Adenosine
* Adenosine A2 Receptor Agonists
* Adenosine A2 Receptor Antagonists
* Adenylyl Cyclase Inhibitors
* Adenylyl Cyclases
* Aging
* Animals
* Arterioles
* Cell Membrane Permeability
* Dose-Response Relationship, Drug
* Enzyme Inhibitors
* Female
* Gene Expression Regulation
* Muscle, Skeletal
* Phenethylamines
* RNA, Messenger
* Rats
* Rats, Sprague-Dawley
* Receptor, Adenosine A1
* Receptor, Adenosine A2A
* Receptor, Adenosine A2B
* Serum Albumin
* Triazines
* Triazoles
* Vasodilator Agents
* Venules

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459528
}}
{{medline-entry
|title=Aging impairs endothelium-dependent vasodilation in rat skeletal muscle arterioles.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/12234821
|abstract=Blood flow capacity in skeletal muscle declines with age. Reduced blood flow capacity may be related to decline in the maximal vasodilatory capacity of the resistance vasculature. This study tested the hypothesis that aging results in impaired vasodilatory capacity of first-order (1A) arterioles isolated from rat-hindlimb locomotory muscle: 1A arterioles (90-220 microm) from gastrocnemius and soleus muscles of young (4 mo) and aged (24 mo) Fischer-144 rats were isolated, cannulated, and pressurized via hydrostatic reservoirs. Vasodilatory responses to increasing concentrations of ACh (10(-9) to 10(-4) M), adenosine ([[ADO]], 10(-10) to 10(-4) M), and sodium nitroprusside (SNP, 10(-10) to 10(-4) M) were evaluated at a constant intraluminal pressure of 60 cmH(2)O in the absence of flow. Flow-induced vasodilation was also evaluated in the absence of pressure changes. Responses to [[ADO]] and SNP were not altered by age. Endothelium-dependent vasodilation induced by flow was significantly reduced in arterioles from both gastrocnemius and soleus muscles. In contrast, endothelium-dependent vasodilation to ACh was reduced only in soleus muscle arterioles. These results indicate that aging impairs vasodilatory responses mediated through the endothelium of resistance arterioles from locomotory muscle, whereas smooth muscle vasodilatory responses remain intact with aging. Additionally, ACh-induced vasodilation was altered by age only in soleus muscle arterioles, suggesting that the mechanism of age-related endothelial impairment differs in arterioles from soleus and gastrocnemius muscles.
|mesh-terms=* Acetylcholine
* Adenosine
* Aging
* Animals
* Arterioles
* Cyclooxygenase Inhibitors
* Endothelium, Vascular
* Enzyme Inhibitors
* Indomethacin
* Male
* Muscle, Skeletal
* NG-Nitroarginine Methyl Ester
* Nitric Oxide
* Nitric Oxide Synthase
* Nitroprusside
* Rats
* Rats, Inbred F344
* Stress, Mechanical
* Vasodilation
* Vasodilator Agents
|keywords=Non-programmatic
|full-text-url=https://sci-hub.do/10.1152/ajpheart.00004.2002
}}
{{medline-entry
|title=Adenosine-enhanced ischemic preconditioning provides enhanced cardioprotection in the aged heart.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/9930490
|abstract=Recently we have reported a novel myo-protective protocol "adenosine-enhanced ischemic preconditioning" ([[APC]]), which extends and amends the protection afforded by ischemic preconditioning (IPC) by both reducing myocardial infarct size and enhancing postischemic functional recovery in the mature rabbit heart. However, the efficacy of [[APC]] in the senescent myocardium was unknown. The efficacy of [[APC]] was investigated in senescent rabbit hearts and compared with magnesium-supplemented potassium cardioplegia (K/Mg) and IPC. Global ischemia (GI) hearts were subjected to 30 minutes of global ischemia and 120 minutes of reperfusion. Ischemic preconditioning hearts received 5 minutes of global ischemia and 5 minutes of reperfusion before global ischemia. Magnesium-supplemented potassium cardioplegia hearts received cardioplegia just before global ischemia. Adenosine-enhanced ischemic preconditioning hearts received a bolus injection of adenosine in concert with IPC. To separate the effects of adenosine from that of [[APC]], a control group ([[ADO]]) received a bolus injection of adenosine 10 minutes before global ischemia. Infarct size was significantly decreased to 18.9% /-2.7% with IPC (p<0.05 versus GI); 17.0% /-1.0% with [[ADO]] (p<0.05 versus GI); 7.7% /-1.3% with K/Mg (p<0.05 versus GI, IPC, and [[ADO]]); and 2.1% /-0.6% with [[APC]] (p<0.05 versus GI, IPC, [[ADO]], and K/Mg; not significant versus control). Only [[APC]] and K/Mg significantly enhanced postischemic functional recovery (not significant versus control). Adenosine-enhanced ischemic preconditioning provides similar protection to K/Mg cardioplegia, significantly enhancing postischemic functional recovery and decreasing infarct size in the senescent myocardium.
|mesh-terms=* Adenosine
* Aging
* Animals
* Cardioplegic Solutions
* Heart Arrest, Induced
* Ischemic Preconditioning, Myocardial
* Magnesium
* Myocardial Reperfusion Injury
* Potassium
* Rabbits
* Vasodilator Agents

|full-text-url=https://sci-hub.do/10.1016/s0003-4975(98)01042-x
}}