Responsiveness to adenosine diphosphate on carotid arterial and platelet functions in type 2 diabetic Otsuka Long-Evans Tokushima Fatty rats.

Authors

Hideaki Tagashira, Kumiko Taguchi, Takayuki Nagano, Tsuneo Kobayashi, Hiroaki Kimura, Naoko Tanaka-Totoribe, Takayuki Matsumoto

Published in

Purinergic signalling. Volume 22. Issue 4. Jun 27, 2026. Epub Jun 27, 2026.

Abstract

Extracellular nucleotides, including adenosine diphosphate (ADP), are pivotal in regulating vascular and platelet function. Thus, their abnormal function contributes significantly to the initiation and progression of diabetic complications. This study investigated ADP-induced changes in carotid arterial responses and platelet aggregation in type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. In the carotid arteries, ADP- and sodium nitroprusside (SNP)-induced relaxations were similar between OLETF rats and Long-Evans Tokushima Otsuka (LETO) rats. However, acetylcholine (ACh)-induced relaxation was lower in OLETF rats than in LETO rats. The prostacyclin analog beraprost did not induce relaxation in both groups. Under nitric oxide synthase inhibition, both ADP- and ACh-induced relaxation were eliminated in both rat groups. Under cyclooxygenase inhibition, ADP-induced relaxation was comparable between the groups, whereas ACh-induced relaxation was lower in OLETF rats than in LETO rats. ADP-induced platelet aggregation was greater in OLETF rats than in LETO rats, whereas collagen-induced aggregations was similar between the two groups. Beraprost suppressed both ADP- and collagen-induced aggregation in each group, while diminishing group differences in ADP-induced platelet aggregation. SNP did not affect either ADP- or collagen-induced platelet aggregation in both groups. Overall, these results demonstrate that responsiveness to ADP was preserved in the carotid arteries but was augmented in platelets in OLETF rats. These different ADP-induced reactivities may provide important clues for elucidating the mechanisms of diabetes-associated complications.

PMID:
42371212
Bibliographic data and abstract were imported from PubMed on 29 Jun 2026.

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