Pharmacology of adenosine receptors in the vasculature

Control of Adenosine Transport by Hypoxia

“…Alternatively, adenosine can be generated from hydrolysis of S-adensylhomocysteine by S-adenosylhomocysteine hydrolase. 6 On the other hand, adenosine deaminase which is widely distributed in many cells and tissues converts adenosine to inosine, whereas adenosine kinase catalyzes the formation of AMP from adenosine. 6 Hypoxia leads to the breakdown of ATP resulting in nucleotide catabolism predominantly via dephosphorylation of AMP by 5Ј-nucleotidases.…”

“…6 On the other hand, adenosine deaminase which is widely distributed in many cells and tissues converts adenosine to inosine, whereas adenosine kinase catalyzes the formation of AMP from adenosine. 6 Hypoxia leads to the breakdown of ATP resulting in nucleotide catabolism predominantly via dephosphorylation of AMP by 5Ј-nucleotidases. 3 Hypoxia can upregulate an adenine nucleotide-metabolizing ecto-enzyme cascade comprising ecto-ATP apyrase (CD39) and CD73, whereby de novo synthesis of functional active CD73 is dependent on the hypoxia-inducible transcription factor HIF-1␣.…”

“…6 In human umbilical vein endothelial cells (HUVEC), adenosine is generated continuously but is immediately recycled via adenosine kinase thus leaving the cytosolic adenosine concentrations low and allowing adenosine uptake. 1 The capacity to take up adenosine from the extracellular space plays a prominent role in adenosine homeostasis.…”

Ecto‐5′‐Nucleotidase‐Positive Cells in the Choroid and Ciliary Body of the Rat Eye

“…In the kidney, it constricts afferent arterioles and reduces glomerular filtration rate, whereas in deep renal cortex and medulla it causes vasodilation (Vallon et al, 2006). In the heart, adenosine is a potent vasodilator of coronary arteries of many species (e.g., rabbits, rats, and dogs) (Tabrizchi and Bedi, 2001). In the pulmonary circulation, adenosine can cause contraction or relaxation depending on the basal vessel tone and on the activation of A1 (vasoconstriction) or A2 (vasodilation) receptors (Cheng et al, 1996).…”

Mécanismes de l’effet diurétique de la caféine

“…Au niveau cardiovasculaire, la caféine exerce un effet chronotrope positif par antagonisme du récepteur A1, étant ainsi responsable d'une tachycardie sympto matique lors d'une ingestion de doses supérieures à 500 mg. Cet effet inotrope positif 3 s'explique par l'aug mentation de l'entrée intracellulaire de Ca 2+ durant le potentiel d'action [6]. Au niveau vasculaire, en fonc tion de la prédominance tissulaire des récepteurs A1 ou des récepteurs A2, la caféine peut provoquer soit une vasoconstriction, soit une vasodilatation [7]. catécholamines par les glandes surrénales.…”