Purinergic Signaling During Hyperglycemia in Vascular Smooth Muscle Cells

Miguel Martin-Aragon Baudel, Ricardo Espinosa-Tanguma, Madeline Nieves-Cintron, Manuel F. Navedo

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations


The activation of purinergic receptors by nucleotides and/or nucleosides plays an important role in the control of vascular function, including modulation of vascular smooth muscle excitability, and vascular reactivity. Accordingly, purinergic receptor actions, acting as either ion channels (P2X) or G protein-coupled receptors (GCPRs) (P1, P2Y), target diverse downstream effectors, and substrates to regulate vascular smooth muscle function and vascular reactivity. Both vasorelaxant and vasoconstrictive effects have been shown to be mediated by different purinergic receptors in a vascular bed- and species-specific manner. Purinergic signaling has been shown to play a key role in altering vascular smooth muscle excitability and vascular reactivity following acute and short-term elevations in extracellular glucose (e.g., hyperglycemia). Moreover, there is evidence that vascular smooth muscle excitability and vascular reactivity is severely impaired during diabetes and that this is mediated, at least in part, by activation of purinergic receptors. Thus, purinergic receptors present themselves as important candidates mediating vascular reactivity in hyperglycemia, with potentially important clinical and therapeutic potential. In this review, we provide a narrative summarizing our current understanding of the expression, function, and signaling of purinergic receptors specifically in vascular smooth muscle cells and discuss their role in vascular complications following hyperglycemia and diabetes.

Original languageEnglish (US)
Article number329
JournalFrontiers in Endocrinology
StatePublished - May 22 2020


  • diabetes
  • ion channels
  • myogenic tone
  • P2Y
  • purinergic receptors
  • vascular reactivity

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism


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