Diabetes Affects the A1 Adenosine Receptor-Dependent Action of Diadenosine Tetraphosphate (Ap4A) on Cortical and Medullary Renal Blood Flow

2020 ◽  
pp. 1-11
Author(s):  
Ewelina Kreft ◽  
Kornelia Sałaga-Zaleska ◽  
Monika Sakowicz-Burkiewicz ◽  
Kamil Dąbkowski ◽  
Miroslawa Szczepánska-Konkel ◽  
...  
Keyword(s):  
Blood Perfusion ◽  
Diabetic Rats ◽  
Doppler Flowmetry ◽  
Protein Levels ◽  
Microvascular Response ◽  
Adenosine A1 ◽  
Early Increase ◽  
A1 Receptor ◽  
Renal Microvasculature ◽  
Relaxing Effect

Diabetes through adenosine A1 receptor (A<sub>1</sub>R) and P2 receptors (P2Rs) may lead to disturbances in renal microvasculature. We investigated the renal microvascular response to Ap<sub>4</sub>A, an agonist of P2Rs, in streptozotocin-induced diabetic rats. Using laser Doppler flowmetry, renal blood perfusion (RBP) was measured during infusion of Ap<sub>4</sub>A alone or in the presence of A<sub>1</sub>R antagonist, either DPCPX (8-cyclopentyl-1,3-dipropylxanthine) or 8-cyclopentyltheophylline (CPT). Ap<sub>4</sub>A induced a biphasic response in RBP: a phase of rapid decrease was followed by a rapid increase, which was transient in diabetic rats but extended for 30 min in nondiabetic rats. Phase of decreased RBP was not affected by DPCPX or CPT in either group. Early and extended increases in RBP were prevented by DPCPX and CPT in nondiabetic rats, while in diabetic rats, the early increase in RBP was not affected by these antagonists. A<sub>1</sub>R mRNA and protein levels were increased in isolated glomeruli of diabetic rats, but no changes were detected in P2Y<sub>1</sub>R and P2Y<sub>2</sub>R mRNA. Presence of unblocked A<sub>1</sub>R is a prerequisite for the P2R-mediated relaxing effect of Ap<sub>4</sub>A in nondiabetic conditions, but influence of A<sub>1</sub>R on P2R-mediated renal vasorelaxation is abolished under diabetic conditions.

Increase in adenosine A1 receptor gene expression in the liver of streptozotocin-induced diabetic rats

2003 ◽  
Vol 19 (3) ◽  
pp. 209-215 ◽  
Author(s):  
I. M. Liu ◽  
T. F. Tzeng ◽  
C. C. Tsai ◽  
T. Y. Lai ◽  
C. T. Chang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Receptor Gene ◽  
Diabetic Rats ◽  
Adenosine A1 Receptor ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Receptor Gene Expression

Adenosine A1 Receptor Antagonist Up-regulates Casp3 and Stimulates Apoptosis Rate in Breast Cancer Cell Line T47D

2020 ◽  
Vol 9 (1) ◽  
pp. 14-20
Author(s):  
Mohammad Zamani Rarani ◽  
Fahimeh Zamani Rarani ◽  
Ali Valiani ◽  
Zeinolabedin Shrifian Dastjerdi ◽  
Elias Kargar Abargouei ◽  
...  
Keyword(s):  
Cell Line ◽  
Cancer Cell Line ◽  
P53 Gene ◽  
T47d Cell ◽  
Adenosine A1 Receptor ◽  
T47d Cells ◽  
Apoptosis Rate ◽  
Adenosine A1 ◽  
T47d Cell Line ◽  
A1 Receptor

Background: Adenosine receptor family, especially A1 type is-overexpressed in breast-derived tumor cells and the P53 gene is mutant in some of these cells while the casps gene is of wild type as well. The aim of this study was to evaluate the effect of the A1 receptor function on cell programmed death or proliferation, as well as the relationship between this receptor stimulation/inhibition and caspase 3 (casp3) expression in T47D cell line that has a mutant and non-functional P53 gene. Materials and Methods: The expression of casps3 was measured by real-time polymerase chain reaction and then flow cytometery and MTT assay were used to assess the apoptotic and proliferation cell rate after the treatment of T47D cells with specific agonist N6-cyclopentyladenosine (CPA) and antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) of this receptor 24, 48, and 72 hours after treatment. Result: Our results indicated that DPCPX significantly induces apoptosis in T47D cells and the rate of survival cell after the reduction of this treatment, especially 72 hours after treatment. Finally, the expression of casp3 was up-regulated by DPCPX treatment, especially in 72 hours while CPA treatment had opposite results (P>0.05). Conclusion: In general, DPCPX could up-regulate casp3 gene expression and subsequently increase the apoptosis rate in T47D cells with casp3 expression without the P53 gene interference. Therefore, adenosine A1 receptor antagonists may be introduced as anti-cancer agents.

scholarly journals Mechanisms of Venoarteriolar Reflex in Type 2 Diabetes with or without Peripheral Neuropathy

Biology ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 333
Author(s):  
Cécile Reynès ◽  
Antonia Perez-Martin ◽  
Houda Ennaifer ◽  
Henrique Silva ◽  
Yannick Knapp ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Peripheral Neuropathy ◽  
Spectral Power ◽  
Blood Perfusion ◽  
Doppler Flowmetry ◽  
Relative Contribution ◽  
Total Spectral Power ◽  
Underlying Mechanisms ◽  
Endothelial Nitric Oxide

The aim of this study is to investigate the underlying mechanisms of the venoarteriolar reflex (VAR) in type 2 diabetes mellitus (T2DM), with and without peripheral neuropathy. Laser Doppler flowmetry (LDF) recordings were performed on the medial malleus and dorsal foot skin, before and during leg dependency in healthy controls, in persons with obesity, in those with T2DM, in those with T2DM and subclinical neuropathy, and in those with T2DM and confirmed neuropathy. LDF recordings were analyzed with the wavelet transform to evaluate the mechanisms controlling the flowmotion (i.e., endothelial nitric oxide-independent and -dependent, neurogenic, myogenic, respiratory and cardiac mechanisms). Skin blood perfusion decreased throughout leg dependency at both sites. The decrease was blunted in persons with confirmed neuropathy compared to those with T2DM alone and the controls. During leg dependency, total spectral power increased in all groups compared to rest. The relative contribution of the endothelial bands increased and of the myogenic band decreased, without differences between groups. Neurogenic contribution decreased in controls, in persons with obesity and in those with T2DM, whereas it increased in subclinical- and confirmed neuropathy. In conclusion, this study provides evidence that confirmed diabetic neuropathy alters the VAR through the neurogenic response to leg dependency.

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