Oxytocin induces intracellular Ca2+ release in cardiac fibroblasts from neonatal rats

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


Pituitary neuropeptide oxytocin is increasingly recognised as a cardiovascular hormone, in addition to its many regulatory roles in other organ systems. Studies in atrial and ventricular myocytes from the neonatal and adult rats have identified synthesis of oxytocin and the expression of oxytocin receptors in these cells. In cardiac fibroblasts, the most populous non-myocyte cell type in mammalian heart, the oxytocin receptors have not been described before. In the present study, we have investigated the direct effects of oxytocin on intracellular Ca2+ dynamics in ventricular myocytes and fibroblasts from new born rats. In myocytes, oxytocin increased the frequency of spontaneous Ca2+ transients and decreased their amplitude. Our data suggest that oxytocin receptors are also present and functional in the majority of cardiac fibroblasts. We used selective oxytocin receptor inhibitor L-371,257 and a number of intracellular Ca 2+ release blockers to investigate the mechanism of oxytocin induced Ca2+ signalling in cardiac fibroblasts. Our findings suggest that oxytocin induces Ca2+ signals in cardiac fibroblasts by triggering endoplasmic reticulum Ca2+ release via inositol trisphosphate activated receptors. The functional significance of the oxytocin induced Ca2+ signalling in cardiac fibroblasts, especially for their activation into secretory active myofibroblasts, remains to be investigated.

Original languageEnglish
Article number102099
JournalCell Calcium
Publication statusPublished - Dec 2019


  • Calcium signalling
  • Cardiac fibroblasts
  • Endoplasmic reticulum
  • IP3 receptors
  • Oxytocin

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology


Dive into the research topics of 'Oxytocin induces intracellular Ca2+ release in cardiac fibroblasts from neonatal rats'. Together they form a unique fingerprint.

Cite this