Proceedings of The Physiological Society

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, PCA367

Poster Communications

Role of Nitric Oxide in the control of the SR Ca2+ release in myocytes of arteriolar networks in situ

L. Borysova1, S. Wray1, D. A. Eisner2, T. Burdyga1

1. Department of Cellular and Molecular Physiology, University of Liverpool, Liverpool, United Kingdom. 2. Unit of Cardiac Physiology, University of Manchester, Manchester, United Kingdom.


NO/cGMP signalling pathway represents one of the possible cross-talk mechanisms between myocytes and endothelial cells in macro- and microvessels. Recent data suggest that NO plays a key role in control of Ca2+ release from ryanodine- and IP3- sensitive Ca2+ stores. The functional link between Ca2+ release and IP3R phosphorylation has been established. These data suggest that Ca2+ oscillations mediated by IP3 and/or RyR channels could be potential targets of NO/cGMP pathway. In our recent work we have established that in myocytes of arcade arterioles there are two independent Ca2+ stores: one is sensitive to caffeine/ryanodine and the other to agonist/2-APB. In the present work we used 2-and 3-dimensional live confocal imaging of ureteric microvascular networks in situ to investigate interaction between endothelium Ca2+ signalling and Ca2+ signalling in myocytes induced by [Arg8]-Vasopressin (AVP, 5nM) and caffeine (0.5-2mM) of all sections of arteriolar networks. Caffeine induced irregular Ca2+ oscillations exclusively in myocytes of arcade arterioles, which appeared as propagating Ca2+ waves with variable spatial spread, selectively blocked by ryanodine (50µM). AVP induced Ca2+ oscillations in all sections of arteriolar network, which appeared as fully propagating recurrent Ca2+ waves. Ryanodine had no effect on AVP-induced Ca2+ oscillations in myocytes of all sections of arteriolar network, selectively inhibited by 2-APB (50 µM). Activation of endothelial Ca2+ signalling by 1µM CCh produced complete termination of the AVP-induced Ca2+ oscillations in myocytes of all sections of arteriolar network but had no effects on Ca2+ sparks and caffeine-induced Ca2+ oscillations in myocytes of arcade arterioles. L-NAME but not indomethacin prevented the inhibitory effect of endothelial Ca2+ signalling on AVP-induced Ca2+ oscillations in myocytes, suggesting that NO was involved. NO donor SNAP (20 µM) or SNP (20µM) produced quick and reversible inhibition of AVP-induced Ca2+ oscillations in myocytes of all sections of arteriolar network but had no effect on Ca2+ sparks and caffeine-induced Ca2+ oscillations in myocytes of arcade arterioles. The data obtained suggest that L-Arginine/NO pathway controls agonist induced Ca2+ oscillations in myocytes of arteriolar networks by selective inhibition of Ca2+ release via IP3R channels.

Where applicable, experiments conform with Society ethical requirements