Myocardial and Plasma Levels of Adenosine 3′:5′-Cyclic Phosphate

Rabinowitz, Babeth; Parmley, William W.; Kligerman, Miriam; Norman, Jim; Fujimura, Shigefumi; Chiba, Shuya; Matloff, Jack M.

doi:10.1378/chest.68.1.69

Cited by 16 publications

(7 citation statements)

References 23 publications

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“…Plasma and tissue levels of cAMP-elevating agonists, including catecholamines and adrenomedullin, rapidly increase in many organs, including the heart, after injury (13). TGF␤1 expression increases at wound sites 1-3 days after myocardial infarction (29).…”

Section: Discussionmentioning

confidence: 99%

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The cyclic AMP effector Epac integrates pro- and anti-fibrotic signals

Yokoyama¹,

Patel²,

Lai

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

132

167

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Scar formation occurs during the late stages of the inflammatory response but, when excessive, produces fibrosis that can lead to functional and structural damage of tissues. Here, we show that the profibrogenic agonist, transforming growth factor β1, transcriptionally decreases expression of Exchange protein activated by cAMP 1 (Epac1) in fibroblasts/fibroblast-like cells from multiple tissues (i.e., cardiac, lung, and skin fibroblasts and hepatic stellate cells). Overexpression of Epac1 inhibits transforming growth factor β1-induced collagen synthesis, indicating that a decrease of Epac1 expression appears to be necessary for the fibrogenic phenotype, an idea supported by evidence that Epac1 expression in cardiac fibroblasts is inhibited after myocardial infarction. Epac and protein kinase A, a second mediator of cAMP action, have opposite effects on migration but both inhibit synthesis of collagen and DNA by fibroblasts. Epac is preferentially activated by low concentrations of cAMP and stimulates migration via the small G protein Rap1 but inhibits collagen synthesis in a Rap1-independent manner. The regulation of Epac expression and activation thus appear to be critical for the integration of pro- and anti-fibrotic signals and for the regulation of fibroblast function.

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Section: Discussionmentioning

confidence: 99%

“…Intracellular cAMP levels evoke numerous cellular responses after cardiac injury (13,14). The role of Epac in cardiac injury and repair is not known, although Epac activation can influence other aspects of cardiac function (15).…”

mentioning

confidence: 99%

The cyclic AMP effector Epac integrates pro- and anti-fibrotic signals

Yokoyama¹,

Patel²,

Lai

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

132

167

View full text Add to dashboard Cite

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“…Studies have demonstrated that clamping or transection of the aorta in dogs (41,42) or in rats (18,43) increases cyclic AMP, an effect abolished by ,Breceptor blockade (18,(41)(42)(43); and anoxia increases rat heart cyclic AMP (16)(17)(18)) also blocked by 1-receptor blockade (17,18). However, these changes have not been related previously to electrophysiological events subsequent to ischemia.…”

Section: Resultsmentioning

confidence: 99%

Mechanisms Contributing to Malignant Dysrhythmias Induced by Ischemia in the Cat

Corr¹,

Witkowski²,

Sobel³

1978

J. Clin. Invest.

157

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“…74, No. In dogs insignificant changes of venous cyclic AMP were found after localized coronary occlusion (26). In dogs insignificant changes of venous cyclic AMP were found after localized coronary occlusion (26).…”

Section: Discussionmentioning

confidence: 91%

“…The increase in myocardial cyclic-AMP levels following ischemia or coronary occlusion (14,(24)(25)(26) is induced by release of catecholamines within the cardiac tissue and activation of adenyl cyclase. Venous plasma cyclic AMP is increased slightly after coronary occlusion in dogs (26) as well as in patients with acute myocardial infarction (24)(25).…”

Section: Discussionmentioning

confidence: 99%

Myocardial extraction of cyclic AMP during pacing-induced angina

Kugler¹,

Nolde²

1979

Basic Res Cardiol

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The application of cyclic AMP as a marker of myocardial ischemia in humans with coronary artery disease has been investigated during pacing-induced angina. Cyclic AMP was determined by a radioimmunoassay. In 15 patients myocardial lactate extraction at rest (20 +/- 12%) converted to production levels (-30 +/- 23%) during angina (p less than 0.0005). Insignificant changes occurred in coronary venous plasma cyclic-AMP levels. The mean myocardial cyclic-AMP extraction at rest (0.3 +/- 8.7%) converted to small release values (-6.0 +/-11%) during angina (= n.s.). No significant correlation was found between myocardial lactate and cyclic-AMP uptake or release. Therefore, cyclic AMP is an insensitive marker in the evaluation of myocardial ischemia.

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Myocardial and Plasma Levels of Adenosine 3′:5′-Cyclic Phosphate

Cited by 16 publications

References 23 publications

The cyclic AMP effector Epac integrates pro- and anti-fibrotic signals

The cyclic AMP effector Epac integrates pro- and anti-fibrotic signals

Mechanisms Contributing to Malignant Dysrhythmias Induced by Ischemia in the Cat

Myocardial extraction of cyclic AMP during pacing-induced angina

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