AMPD1 gene polymorphism and the vasodilatory response to ischemia

Hand, Brian D.; Roth, Stephen M.; Roltsch, Mark H.; Park, Jung Jun; Kostek, Matthew C.; Ferrell, Robert E.; Brown, Michael D.

doi:10.1016/j.lfs.2006.04.003

Cited by 9 publications

(7 citation statements)

References 34 publications

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“…Similarly, no association between the polymorphism and weight (total and fat-free) or BMI was found in another group of young (20-43 years), healthy, nonobese (BMIv30) subjects [22]. However, in the group of young healthy Caucasian females (18 to 35 years of age) the trend (p50.12) towards lower percent body fat in T allele carriers was observed [23], which would be consistent with our results. The waist circumference was not assessed in any of the available studies, although this parameter is the morphometric criterion of the current definition of metabolic syndrome and in our study much more strongly dependent on AMPD1 genotype than BMI.…”

Section: Ampd1 and Obesitysupporting

confidence: 90%

Association of C34TAMPD1gene polymorphism with features of metabolic syndrome in patients with coronary artery disease or heart failure

Safranow¹,

Czyżycka²,

Bińczak-Kuleta³

et al. 2009

Scandinavian Journal of Clinical and Laboratory Investigation

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C34T AMPD1 polymorphism may be associated with reduced frequency of obesity in CAD patients and of hyperglycaemia and diabetes in both CAD and HF patients. Morphometric parameters associated with adipose tissue distribution and parameters of glucose metabolism should be analysed as potential confounders in further studies on the role of polymorphisms of AMPD1 and other genes associated with AMP and adenosine metabolism in cardiovascular disease.

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Section: Ampd1 and Obesitysupporting

confidence: 90%

Association of C34TAMPD1gene polymorphism with features of metabolic syndrome in patients with coronary artery disease or heart failure

Safranow¹,

Czyżycka²,

Bińczak-Kuleta³

et al. 2009

Scandinavian Journal of Clinical and Laboratory Investigation

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“…With respect to AMPD1, the present Wndings are in agreement with two recent studies that have shown augmented hyperaemia in response to forearm ischemia induced by arterial occlusion in C34>T heterozygotes as compared to normal homozygotes (Hand et al 2006;Riksen et al 2007). Current evidence suggests, however, that the augmented hyperaemic response to transient arterial occlusion reported in these studies is mediated by a mechanism diVerent from that underlying the hyperaemic response to exercise observed in the present study (Marshall 2007).…”

supporting

confidence: 93%

“…In exercise induced hyperaemia, adenosine is generated within the skeletal muscle Wbres and, after being released into the interstitial Xuid, acts on A 2A receptors on smooth muscle cells, while during hypoxia adenosine is largely released by endothelial cells and acts on A 1 receptors in a nitric oxide dependent manner. Previous studies have demonstrated accumulation of AMP and IMP in skeletal muscle during exhaustive exercise, indicating an activation of mAMPD, while the transient arterial occlusion investigated in the above-mentioned studies (Hand et al 2006;Riksen et al 2007) can not be expected to cause comparable metabolic changes in skeletal muscle. Furthermore, it has been suggested that adenosine is generated mainly within the vascular compartment during ischemia induced by arterial occlusion, possibly by endothelial cells (Costa et al 1999).…”

mentioning

confidence: 78%

The effect of AMPD1 genotype on blood flow response to sprint exercise

Norman

Nygren²,

Nowak

et al. 2008

Eur J Appl Physiol

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Inherited deficiency of skeletal muscle myoadenylate deaminase (mAMPD) is a genetic disorder characterized primarily by a 34C>T transition in exon 2 of the AMPD1 gene. mAMPD deficient individuals exhibit alterations in ATP catabolic flow, resulting in greater adenosine accumulation during high intensity exercise that may possibly enhance exercise-induced hyperaemia. This study tested the hypothesis that individuals with diminished mAMPD activity due to mutations in the AMPD1 gene develop a greater and faster blood flow response to high intensity exercise than individuals with two AMPD1 normal alleles (NN). Four 34C>T homozygotes, two compound heterozygotes (34C>T in one allele and a recently identified 404delT mutation in the other AMPD1 allele), collectively termed MM, one 34C>T heterozygote (NM) and eight NN males were studied. They performed a 30 s Wingate cycling test with monitoring of power output and other parameters of exercise performance. Common femoral artery blood flow was measured before and after (up to 25 min) exercise, using ultrasonography. Mean power during Wingate cycling was approximately 10% lower in MM/NM than in NN; p<0.01. Blood flow response to exercise also differed between MM/NM and NN individuals (ANOVA; p<0.001). There was also a difference in peak post-exercise blood flow (p<0.05), and the subsequent fall in blood flow during the recovery phase (T1/2) occurred more than twice as fast in MM/NM compared to NN subjects (7.8+/-1.1 min vs. 16.1+/-1.4 min, p<0.001). These results suggest a better circulatory adaptation to exercise in individuals with diminished mAMPD activity, probably due to an AMPD1 genotype-dependent increase in adenosine formation.

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“…After this period of ischemia, the wrist cuff was inflated again and the arm was inflated to 55 mmHg, every minute 24 . It has been shown that the tissue has the ability to recover from ischemia in three minutes and that peak vasodilation occurs in about one minute after the release of the cuff 24,25 . Thus, BF was measured at rest (BF-0) and one, two and three minutes of reactive hyperemia (BF-1 BF-2 and BF-3, respectively), after 5 minutes of ischemia.…”

Section: Basic Testsmentioning

confidence: 99%