Effect of i.v. dipyridamole on cerebral blood flow, blood pressure, plasma adenosine and cAMP levels in rabbits

Hegedüs, Katalin; Keresztes, T.; Fekete, István; Molńar, László

doi:10.1016/s0022-510x(96)05352-x

Cited by 22 publications

(16 citation statements)

References 60 publications

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“…107 In addition to causing vasodilation, dipyridamole is also known to inhibit platelet aggregation and proliferation of vascular smooth muscle cells, and to prevent reactive oxygen species generation by neutrophils. 108 These effects can be attributed to the inhibition of adenosine reuptake into cells and thus increased adenosine signaling. As mentioned, adenosine acts as a vasodilator through the activation of A 2A AdoR 98 or A 2B AdoR.…”

Section: Pharmacological Relevance Of Vascular Nts As Cardiovascular mentioning

confidence: 99%

“…100 Previous studies suggest that dipyridamole can be used to decrease mean arterial blood pressure, although it is not clear whether this is only dependent on adenosine uptake inhibition or on increased cAMP levels attributable to dipyridamole. 108 The fact that decrease in blood pressure is not a clinical observation in dipyridamole-treated patients is probably caused by the short effect of the drug on increasing the plasma adenosine concentration. Mean arterial pressure is the decreased Ϸ10 minutes after drug administration and returns to baselines within 40 minutes.…”

Section: Pharmacological Relevance Of Vascular Nts As Cardiovascular mentioning

confidence: 99%

“…Mean arterial pressure is the decreased Ϸ10 minutes after drug administration and returns to baselines within 40 minutes. 108 More recently, possible new vasodilative drugs have been identified. Thiazolidinediones are a new class of anti-diabetic agents that also have vasodilatory and anti-proliferative effects on vascular smooth muscle cells.…”

Section: Pharmacological Relevance Of Vascular Nts As Cardiovascular mentioning

confidence: 99%

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Physiological Roles of Vascular Nucleoside Transporters

Löffler

Morote-García

Eltzschig

et al. 2007

ATVB

147

124

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Abstract-Nucleoside transporters (NTs) comprise 2 widely expressed families, the equilibrative nucleoside transporters (diffusion-limited channels) and concentrative nucleoside transporters (sodium-dependent transporters). Because of their anatomic position at the blood-tissue interface, vascular NTs are in an ideal position to influence vascular nucleoside levels, particularly adenosine, which among others plays an important role in tissue protection during acute injury. For example, endothelial NTs contribute to preserving the vascular integrity during conditions of limited oxygen availability (hypoxia). Indeed, hypoxia-inducible factor-1-dependent repression of NTs results in enhanced extracellular adenosine signaling and thus attenuates hypoxia-associated increases in vascular leakage. In addition, vascular NTs also contribute to cardiac ischemic preconditioning, coronary vasodilation, and inhibition of platelet aggregation. Moreover, vascular nucleoside uptake via NTs is important for nucleoside recovery, particularly in cells lacking de novo nucleotide synthesis pathways (erythrocytes, leukocytes). Taken together, vascular NTs are critical in modulating adenosine-mediated responses during conditions such as inflammation or hypoxia. (Arterioscler

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Section: Pharmacological Relevance Of Vascular Nts As Cardiovascular mentioning

confidence: 99%

Section: Pharmacological Relevance Of Vascular Nts As Cardiovascular mentioning

confidence: 99%

Section: Pharmacological Relevance Of Vascular Nts As Cardiovascular mentioning

confidence: 99%

See 1 more Smart Citation

Physiological Roles of Vascular Nucleoside Transporters

Löffler

Morote-García

Eltzschig

et al. 2007

ATVB

147

124

View full text Add to dashboard Cite

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“…[71][72][73] sitagliptin [78,79] IFN-␥ [73,74] vildagliptin [80] lithium [75] (?) Stimulate ADA dipyridamole [65,[81][82][83][84] Inhibit ADA cladribrine [85,86] methotrexate [64] fludarabine [87] pentostatin [88] methotrexate [89] During G-CSF-induced mobilization of HSCs from BM, stimulation and avoidance of inhibition of the DPP-IV-ADA complex are desirable. As can be expected from the symbiotic relationship between the two molecules, inhibiting DPP-IV and ADA will maximize total DPP-IV inhibition.…”

Section: Discussionmentioning

confidence: 99%

“…Circulating levels of adenosine are increased after dipyridamole [81], increasing the ADA substrate available for generation of ammonia in vivo in mice [82], dogs [83], and humans [84].…”

Section: Current Pharmacological Optionsmentioning

confidence: 99%

Conditioning response to granulocyte colony-stimulating factor via the dipeptidyl peptidase IV-adenosine deaminase complex

Focosi

Kast

Galimberti

et al. 2008

Journal of Leukocyte Biology

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G-CSF is routinely used to mobilize hematopoietic stem cells (HSCs) from bone marrow (BM) into peripheral blood before aphaeresis, but HSC harvesting can be suboptimal. On the other hand, transplanted HSCs sometimes fail to engraft a recipient BM microenvironment when G-CSF is used after transplantation, as pushing-CSF will push HSCs away from marrow. So, G-CSF action needs to be potentiated by other drugs. Marrow stromal cells establish a local CXCL12 concentration gradient that is the primary homing signal for HSCs. Pharmacological interventions that modify this gradient, therefore, have potential to help HSC mobilization (by decreasing CXCL12) and engraftment (by increasing CXCL12). CXCL12 inactivation is primarily mediated by dipeptidyl peptidase-IV. We review here the currently available drugs affecting this enzyme that could be used in the clinic to achieve phase-specific help for G-CSF.

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