Adenosine and adenosine receptor-mediated action in coronary microcirculation.

Adenosine is an ubiquitous extracellular signaling molecule and plays a fundamental role in the regulation of coronary microcirculation through activation of adenosine receptors (ARs). Adenosine is regulated by various enzymes and nucleoside transporters for its balance between intra- and extracellular compartments. Adenosine-mediated coronary microvascular tone and reactive hyperemia are through receptors mainly involving AR activation on both endothelial and smooth muscle cells, but also involving interaction among other ARs.

Can the Bone Density Estimated by CBCT Predict the Primary Stability of Dental Implants? A New Measurement Protocol.

Background: The use of dental implants to restore edentulous parts of the jaws is a common and well-documented treatment method. Effective dental implant treatment is known to be affected by both the quality and the quantity of bone required for implant placement, bone quality is a critical factor to consider when predicting stability of implants. Thus, stability of the initial implant and the possibility of early loading could be predicated using cone-beam computed tomography (CBCT) scans and primary stability parameters before implant placement.

Limonene-induced activation of A adenosine receptors reduces airway inflammation and reactivity in a mouse model of asthma.

Animal models of asthma have shown that limonene, a naturally occurring terpene in citrus fruits, can reduce inflammation and airway reactivity. However, the mechanism of these effects is unknown. We first performed computational and molecular docking analyses that showed limonene could bind to both A and A receptors.

Alteration of purinergic signaling in diabetes: Focus on vascular function.

Diabetes is an important risk factor for the development of cardiovascular disease including atherosclerosis and ischemic heart disease. Vascular complications including macro- and micro-vascular dysfunction are the leading causes of morbidity and mortality in diabetes. Disease mechanisms at present are unclear and no ideal therapies are available, which urgently calls for the identification of novel therapeutic targets/agents.

Wannier90 as a community code: new features and applications.

Wannier90 is an open-source computer program for calculating maximally-localised Wannier functions (MLWFs) from a set of Bloch states. It is interfaced to many widely used electronic-structure codes thanks to its independence from the basis sets representing these Bloch states. In the past few years the development of Wannier90 has transitioned to a community-driven model; this has resulted in a number of new developments that have been recently released in Wannier90 v3.

Activation of adenosine A but not A receptors is involved in uridine adenosine tetraphosphate-induced porcine coronary smooth muscle relaxation.

Activation of both adenosine A and A receptors (AR) contributes to coronary vasodilation. We previously demonstrated that uridine adenosine tetraphosphate (UpA) is a novel vasodilator in the porcine coronary microcirculation, acting mainly on AR in smooth muscle cells (SMC). We further investigated whether activation of AR is involved in UpA-mediated coronary SMC relaxation.

Role of angiotensin II type 1 (AT1) and type 2 (AT2) receptors in airway reactivity and inflammation in an allergic mouse model of asthma.

Angiotensin II (Ang II) exerts its effects through two G-protein coupled receptors: angiotensin II type 1 receptors (AT1) and type 2 receptors (AT2). Both these receptor subtypes are poorly understood in asthma. In this study, we investigated effects of AT1 receptor antagonist losartan, novel AT2 receptor agonist novokinin and AT2 receptor antagonist PD 123319 in a mouse model of asthma.

Uridine adenosine tetraphosphate and purinergic signaling in cardiovascular system: An update.

Uridine adenosine tetraphosphate (UpA), biosynthesized by activation of vascular endothelial growth factor receptor (VEGFR) 2, was initially identified as a potent endothelium-derived vasoconstrictor in perfused rat kidney. Subsequently, the effect of UpA on vascular tone regulation was intensively investigated in arteries isolated from different vascular beds in rodents including rat pulmonary arteries, aortas, mesenteric and renal arteries as well as mouse aortas, in which UpA produces vascular contraction. In contrast, UpA produces vascular relaxation in porcine coronary small arteries and rat aortas.

Enhanced A adenosine receptor-induced vascular contractions in mesenteric artery and aorta of in L-NAME mouse model of hypertension.

L-NAME-induced hypertension is commonly used to study endothelial dysfunction and related vascular effects. It has been reported that genetic deletion of A adenosine receptor (AR) reduces blood pressure (BP) increases in mice and thus, suggesting the involvement of AAR. Thus, we sought to determine whether AAR-induced vascular responses were altered in this mouse model of hypertension.

Functional changes in vascular reactivity to adenosine receptor activation in type I diabetic mice.

Activation of adenosine receptors has been implicated in several biological functions, including cardiovascular and renal function. Diabetes causes morphological and functional changes in the vasculature, resulting in abnormal responses to various stimuli. Recent studies have suggested that adenosine receptor expression and signaling are altered in disease states such as hypertension, diabetes.

Divergent coronary flow responses to uridine adenosine tetraphosphate in atherosclerotic ApoE knockout mice.

Uridine adenosine tetraphosphate (UpA) exerts potent relaxation in porcine coronary arteries that is reduced following myocardial infarction, suggesting a crucial role for UpA in the regulation of coronary flow (CF) in cardiovascular disorders. We evaluated the vasoactive effects of UpA on CF in atherosclerosis using ApoE knockout (KO) mice ex vivo and in vivo. Functional studies were conducted in isolated mouse hearts using the Langendorff technique.

Transcriptomic effects of adenosine 2A receptor deletion in healthy and endotoxemic murine myocardium.

Influences of adenosine 2A receptor (AR) activity on the cardiac transcriptome and genesis of endotoxemic myocarditis are unclear. We applied transcriptomic profiling (39 K Affymetrix arrays) to identify AR-sensitive molecules, revealed by receptor knockout (KO), in healthy and endotoxemic hearts. Baseline cardiac function was unaltered and only 37 AR-sensitive genes modified by AR KO (≥1.

In vivo assessment of coronary flow and cardiac function after bolus adenosine injection in adenosine receptor knockout mice.

Bolus injections of adenosine and the A2A adenosine receptor (AR) selective agonist (regadenoson) are used clinically as a substitute for a stress test in people who cannot exercise. Using isolated tissue preparations, our lab has shown that coronary flow and cardiac effects of adenosine are mostly regulated by the AR subtypes A1, A2A, and A2B In this study, we used ultrasound imaging to measure the in vivo effects of adenosine on coronary blood flow (left coronary artery) and cardiac function in anesthetized wild-type, A1 knockout (KO), A2AKO, A2BKO, A3KO, A1, and A3 double KO (A1/3 DKO) and A2A and A2B double KO (A2A/2B DKO) mice in real time. Echocardiographic and Doppler studies were performed using a Visualsonic Vevo 2100 ultrasound system.

Role of Adenosine Receptor(s) in the Control of Vascular Tone in the Mouse Pudendal Artery.

Activation of adenosine receptors (ARs) has been implicated in the modulation of renal and cardiovascular systems, as well as erectile functions. Recent studies suggest that adenosine-mediated regulation of erectile function is mainly mediated through A2BAR activation. However, no studies have been conducted to determine the contribution of AR subtype in the regulation of the vascular tone of the pudendal artery (PA), the major artery supplying and controlling blood flow to the penis.

Enhanced A2A adenosine receptor-mediated increase in coronary flow in type I diabetic mice.

Adenosine A2A receptor (A2AAR) activation plays a major role in the regulation of coronary flow (CF). Recent studies from our laboratory and others have suggested that A2AAR expression and/or signaling is altered in disease conditions. However, the coronary response to AR activation, in particular A2AAR, in diabetes is not fully understood.

Angiotensin II stimulation alters vasomotor response to adenosine in mouse mesenteric artery: role for A1 and A2B adenosine receptors.

Background And Purpose: Stimulation of the A1 adenosine receptor and angiotensin II receptor type-1 (AT1 receptor) causes vasoconstriction through activation of cytochrome P450 4A (CYP4A) and ERK1/2. Thus, we hypothesized that acute angiotensin II activation alters the vasomotor response induced by the non-selective adenosine receptor agonist, NECA, in mouse mesenteric arteries (MAs).

Experimental Approach: We used a Danish Myo Technology wire myograph to measure muscle tension in isolated MAs from wild type (WT), A1 receptor and A2B receptor knockout (KO) mice.

Theory and computation of hot carriers generated by surface plasmon polaritons in noble metals.

Hot carriers (HC) generated by surface plasmon polaritons (SPPs) in noble metals are promising for application in optoelectronics, plasmonics and renewable energy. However, existing models fail to explain key quantitative details of SPP-to-HC conversion experiments. Here we develop a quantum mechanical framework and apply first-principles calculations to study the energy distribution and scattering processes of HCs generated by SPPs in Au and Ag.

Mechanisms underlying uridine adenosine tetraphosphate-induced vascular contraction in mouse aorta: Role of thromboxane and purinergic receptors.

Uridine adenosine tetraphosphate (Up4A), a novel endothelium-derived vasoactive agent, is proposed to play a role in cardiovascular disorders and induces aortic contraction through activation of cyclooxygenases (COXs). We and others demonstrated that activation of A1 or A3 adenosine receptors (ARs) results in vascular contraction via thromboxane (TX) A2 production. However, the mechanisms of Up4A-induced vascular contraction in mouse aorta are not understood.

Involvement of NADPH oxidase in A2A adenosine receptor-mediated increase in coronary flow in isolated mouse hearts.

Adenosine increases coronary flow mainly through the activation of A2A and A2B adenosine receptors (ARs). However, the mechanisms for the regulation of coronary flow are not fully understood. We previously demonstrated that adenosine-induced increase in coronary flow is in part through NADPH oxidase (Nox) activation, which is independent of activation of either A1 or A3ARs.

High salt diet modulates vascular response in A2AAR (+/+) and A 2AAR (-/-) mice: role of sEH, PPARγ, and K ATP channels.

This study aims to investigate the signaling mechanism involved in HS-induced modulation of adenosine-mediated vascular tone in the presence or absence of adenosine A2A receptor (A2AAR). We hypothesized that HS-induced enhanced vascular relaxation through A2AAR and epoxyeicosatrienoic acid (EETs) is dependent on peroxisome proliferator-activated receptor gamma (PPARγ) and ATP-sensitive potassium channels (KATP channels) in A2AAR(+/+) mice, while HS-induced vascular contraction to adenosine is dependent on soluble epoxide hydrolase (sEH) that degrades EETs in A2AAR(-/-) mice. Organ bath and Western blot techniques were conducted in HS (4 % NaCl) and normal salt (NS, 0.

Metabolic hyperemia requires ATP-sensitive K+ channels and H2O2 but not adenosine in isolated mouse hearts.

We have previously demonstrated that adenosine-mediated H2O2 production and opening of ATP-sensitive K(+) (KATP) channels contributes to coronary reactive hyperemia. The present study aimed to investigate the roles of adenosine, H2O2, and KATP channels in coronary metabolic hyperemia (MH). Experiments were conducted on isolated Langendorff-perfused mouse hearts using combined pharmacological approaches with adenosine receptor (AR) knockout mice.

A₁ adenosine receptor deficiency or inhibition reduces atherosclerotic lesions in apolipoprotein E deficient mice.

Aims: The goal of this study was to determine whether the A1 adenosine receptor (AR) plays a role in atherosclerosis development and to explore its potential mechanisms.

Methods And Results: Double knockout (DKO) mice, deficient in the genes encoding A1 AR and apolipoprotein E (apoE), demonstrated reduced atherosclerotic lesions in aortic arch (en face), aortic root, and innominate arteries when compared with apoE-deficient mice (APOE-KO) of the same age. Treating APOE-KO with an A1 AR antagonist (DPCPX) also led to a concentration-dependent reduction in lesions.

Evidence for the involvement of NADPH oxidase in adenosine receptors-mediated control of coronary flow using A and A knockout mice.

The NADPH oxidase (Nox) subunits 1, 2 (gp91 ) and 4 are the major sources for reactive oxygen species (ROS) in cardiovascular system. In conditions such as ischemia-reperfusion injury and hypoxia, both ROS and adenosine are released suggesting a possible interaction. We hypothesized that ROS generated through Nox is involved in adenosine-induced coronary flow (CF) responses.