Mechanism of vasodilation to adenosine in coronary arterioles from patients with heart disease.

@article{Sato2005MechanismOV,
  title={Mechanism of vasodilation to adenosine in coronary arterioles from patients with heart disease.},
  author={Atsushi Sato and Ken Terata and Hiroto Miura and Kazuyoshi Toyama and Fausto R. Loberiza and Ossama A Hatoum and Takashi Saito and Ichiro Sakuma and David D. Gutterman},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2005},
  volume={288 4},
  pages={
          H1633-40
        },
  url={https://api.semanticscholar.org/CorpusID:71178}
}
Adenosine endothelium independently dilates HCAs from patients with heart disease through a receptor-mediated mechanism that involves the activation of intermediate-conductance K(Ca) channels via an AC signaling pathway.
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60 References

Adenosine A(2A) receptors mediate coronary microvascular dilation to adenosine: role of nitric oxide and ATP-sensitive potassium channels.

Functional and molecular characterization of receptor subtypes mediating coronary microvascular dilation to adenosine.

Results from RT/PCR and in situ hybridization suggest that coronary arteriolar dilation to adenosine is primarily mediated by the opening of K(ATP) channels through activation of A2A receptors.

Human coronary arteriolar dilation to adrenomedullin: role of nitric oxide and K(+) channels.

It is proposed that, in human coronary arterioles, ADM elicits vasodilation in partThrough production of nitric oxide and in part through activation of K(+) channels, with little contribution from adenylyl cyclase.

Pharmacologic activation of the human coronary microcirculation in vitro: endothelium-dependent dilation and differential responses to acetylcholine.

Endogenous adenosine and coronary vasoconstriction in hypoperfused myocardium during exercise.

Endogenous adenosine contributed to dilatation of resistance vessels in hypoperfused myocardium of exercising dogs in the absence as well as in the presence of U46619, and did not attenuate the magnitude of the vasoconstrictor response to U46620.

cAMP-independent dilation of coronary arterioles to adenosine : role of nitric oxide, G proteins, and K(ATP) channels.

The results suggest that adenosine activates both endothelial and smooth muscle pathways to exert its vasodilatory function, and appears that the latter vasodilation process is independent of G proteins and of cAMP/cGMP pathways.

Mechanism of thrombin-induced vasodilation in human coronary arterioles.

Thrombin-induced dilation in human arterioles is independent of G(i)-protein activation and NO release, however, Thromb dilation is endothelium dependent, is maintained on consecutive applications, and involves activation of K(+) channels.

Contribution of adenosine to changes in coronary flow in metabolically stimulated rat heart.

Data show that about a third of the vasodilation that results from the metabolic stimulation of rat heart by catecholamines is due to the receptor-mediated action of extracellular adenosine.

Effect of ATP-Sensitive Potassium Channel Inhibition on Resting Coronary Vascular Responses in Humans

Vascular KATP channels are involved in the maintenance of basal coronary tone but may not be essential to adenosine-induced coronary hyperemia in humans.

Theophylline increases coronary vascular tone in humans: evidence for a role of endogenous adenosine in flow regulation.

The hypothesis that endogenous adenosine is involved in regulation of human coronary tone is supported.
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