Evidence for an A2 adenosine receptor in human coronary arteries

Mv, Ramagopal; Rw, Chitwood; Sj, Mustafa

doi:10.1016/0014-2999(88)90548-1

Cited by 42 publications

(25 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This study also showed that contractile responses of human coronary arteries to α,β-meATP and the stable pyrimidine analogue, uridine 5′-O-3-thiotriphosphate, were consistent with activation of P2X1R and P2Y2R, respectively. UTPevoked contractions of porcine coronary artery smooth muscle cells also appear to be mediated predominantly by P2Y2R [422][423][424][425][426]. The adenosine may be released directly from cardiomyocytes and endothelial cells after intra-and extracellular breakdown of ATP, respectively [427].…”

Section: Coronary Blood Vesselsmentioning

confidence: 99%

Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

120

View full text Add to dashboard Cite

This review is a historical account about purinergic signalling in the heart, for readers to see how ideas and understanding have changed as new experimental results were published. Initially, the focus is on the nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory nerves, as well as in intracardiac neurons. Control of the heart by centers in the brain and vagal cardiovascular reflexes involving purines are also discussed. The actions of adenine nucleotides and nucleosides on cardiomyocytes, atrioventricular and sinoatrial nodes, cardiac fibroblasts, and coronary blood vessels are described. Cardiac release and degradation of ATP are also described. Finally, the involvement of purinergic signalling and its therapeutic potential in cardiac pathophysiology is reviewed, including acute and chronic heart failure, ischemia, infarction, arrhythmias, cardiomyopathy, syncope, hypertrophy, coronary artery disease, angina, diabetic cardiomyopathy, as well as heart transplantation and coronary bypass grafts.

show abstract

Section: Coronary Blood Vesselsmentioning

confidence: 99%

Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

120

View full text Add to dashboard Cite

show abstract

“…The endotheliumdependent effect of ATP is vasodilatation due to its action at P2Y purinoceptors which leads to release of EDRF and/or prostacyclin (De Mey & Vanhoutte, 1981;Gordon & Martin, 1983;Needham et al, 1987;Boeynaems & Pearson, 1990). The vasodilator action of adenosine is mediated by the A2 subclass of the P1 purinoceptor, which stimulates adenylate cyclase (Collis & Brown, 1983;Ramagopal et al, 1988). The location of adenosine receptors has not been well defined and both endothelium-dependent (Gordon & Martin, 1983;Rubanyi & Vanhoutte, 1985) and -independent White & Angus, 1987) responses have been described.…”

Section: Introductionmentioning

confidence: 99%

Endothelium‐dependent and ‐independent effects of exogenous ATP, adenosine, GTP and guanosine on vascular tone and cyclic nucleotide accumulation of rat mesenteric artery

Vuorinen¹,

Pörsti²,

Metsä‐Ketelä³

et al. 1992

British J Pharmacology

View full text Add to dashboard Cite

1 The effects of exogenous guanosine 5'-triphosphate (GTP) and guanosine on vascular tone and cyclic nucleotide accumulation of noradrenaline-precontracted endothelium-intact and endothelium-denuded rat mesenteric artery rings were compared with the effects of the known purinoceptor agonists adenosine 5'-triphosphate (ATP) and adenosine.2 GTP (10pM-1 mM) dose-dependently relaxed endothelium-intact mesenteric artery rings by producing a rapid initial response followed by sustained relaxation resembling the relaxant response to acetylcholine. GTP also slightly relaxed endothelium-denuded artery rings. The acetylcholine-and GTP-induced relaxations of endothelium-intact rings were attenuated by NG-nitro L-arginine methyl ester (L-NAME, 330pM) which attenuation was reversed with L-arginine (1 mM). 3 Guanosine (lOuM-1 mM) relaxed both endothelium-intact and -denuded artery rings in a dosedependent manner. The relaxations were more pronounced in endothelium-intact preparations and were only slightly attenuated by L-NAME (330pM). 4 ATP (1 pM-1 mM) and adenosine (1OpM-1 mM) dose-dependently relaxed endothelium-intact and -denuded artery rings. The responses were more pronounced in endothelium-intact vascular preparations.5 GTP (100pM) and guanosine (100puM) increased guanosine 3':5'-cyclic monophosphate (cyclic GMP) accumulation in both endothelium-intact and -denuded artery rings corresponding to the relaxations observed. The concentrations of adenosine 3': 5'-cyclic monophosphate (cyclic AMP) were not affected. 6 ATP (100pM) increased cyclic GMP concentration of endothelium-intact artery rings. The concentrations of cyclic AMP were not affected by ATP (100pM) and adenosine (100pM) in endothelium-intact and -denuded vascular preparations. 7 These results provide evidence that exogenous GTP and guanosine relax precontracted endotheliumintact and -denuded rat mesenteric artery rings by increasing cyclic GMP accumulation. The response to GTP of endothelium-intact rings can mainly be explained by the release of endothelium-derived relaxing factor (EDRF), but that of guanosine is only partly due to EDRF, and is a combination of endotheliumdependent and -independent effects. The endothelium-independent response of GTP and guanosine is a direct, unknown effect on smooth muscle and guanylate cyclase.

show abstract

“…At the A1 receptor subtype, N6 substituted analogues, e.g., N6-[l-phenyl-2-propyl]adenosine (PIA), are more potent than 5' substituted analogues, such as 5'-Nethylcarboxamide-adenosine (NECA), with the reverse being true at the A2 receptor subtype. By use of this classification, the presence of A2 subtype receptors has been demonstrated in canine (Kusachi et al, 1983;Nakazawa & Mustafa, 1988), bovine (Mustafa & Askar, 1985) and human coronary arteries (Ramagopal et al, 1988 Ltd, 1990 the rings were stretched to an initial tension of about 1.5 g and allowed to equilibrate and establish baseline tension for 2 to 3 h in the bathing medium, which was changed every 15 min. During this time the preparations were stimulated twice with KC1 (30 mM) and the baseline tension was adjusted to about 1 g. After repeated changes of the bathing solution the tissues were exposed to 3 ,M prostaglandin F2., which induced a stable submaximal contraction of about 80% of maximum response.…”

Section: Introductionmentioning

confidence: 99%

“…In each experiment 6 rings of the same artery were investigated at the same time, one of which was used as a control preparation, to correct for any sensitivity changes during the experiment. (Ramagopal et al, 1988), bovine (Mustafa 8.99 6.34 & Askar, 1985) and monkey coronary arteries (Toda, 1983).…”

Section: Introductionmentioning

confidence: 99%

Characterization of the adenosine receptor in porcine coronary arteries

King

Müller‐Schweinitzer

1990

British J Pharmacology

View full text Add to dashboard Cite

1 Relaxant responses of ring preparations from porcine ventricular coronary arteries to adenosine and various stable adenosine analogues were investigated in vitro. 2 The adenosine analogues did not produce contraction but elicited almost complete relaxation of coronary arteries preconstricted with 3 pJm prostaglandin F2 (PGF2z), even after removal of the endothelium.3 The order of potency, was 5'-N-ethylcarboxamide-adenosine (NECA) > 242-phenylethylamino)5'-adenosine (CPA) > adenosine > ATP = ADP which suggested the presence of adenosine A2-receptor subtypes. 4 There was an excellent correlation between the calculated pD2 values on coronary arteries and the pKD values at adenosine A2 binding sites, whereas no correlation was obtained when the pD2 values were compared to the pKD values at adenosine Al-binding sites on membranes from porcine striata.5 The relaxant effects of adenosine and its analogues were competitively antagonized by 8-(p-sulphophenyl)-theophylline (8-SPT), producing pA2 values similar to the respective pKD value of the antagonist at adenosine A2 binding sites. 6 It is suggested that the porcine coronary artery possesses adenosine A2 receptors which seem to be similar to the adenosine A2 binding site in pig striatum, whereas no evidence was obtained for the presence of adenosine A1 receptors.

show abstract

Evidence for an A2 adenosine receptor in human coronary arteries

Cited by 42 publications

References 5 publications

Cardiac purinergic signalling in health and disease

Cardiac purinergic signalling in health and disease

Endothelium‐dependent and ‐independent effects of exogenous ATP, adenosine, GTP and guanosine on vascular tone and cyclic nucleotide accumulation of rat mesenteric artery

Characterization of the adenosine receptor in porcine coronary arteries

Contact Info

Product

Resources

About