Evidence that NO/cGMP/PKG signalling cascade mediates endothelium dependent inhibition of IP3R mediated Ca(2+) oscillations in myocytes and pericytes of ureteric microvascular network in situ
Abstract
In ureteric microvessels the antagonistic relationship between Ca(2+) signalling in endothelium and Ca(2+) oscillations in myocytes and pericytes of arterioles and venules involves nitric oxide (NO), but the underlying mechanisms are not well understood. In the present study we investigated the effects of carbachol and NO donor SNAP on Ca(2+) signalling and vasomotor responses of arterioles and venules in intact urteric microvascular network in situ using confocal microscopy. Vasomotor responses of arterioles and venules induced by AVP correlated with the occurrence of Ca(2+) oscillations in the myocytes and pericytes and were not abolished by the removal of Ca(2+) from extracellular fluid. Carbachol-induced rise of intracellular Ca(2+) in endothelium was accompanied by the termination of the Ca(2+) oscillations in myocytes and pericytes. This carbachol-induced inhibitory effect on Ca(2+) oscillations in myocytes and pericytes was reversed by ODQ, an inhibitor of soluble guanylyl cyclase (sGC) and by Rp-8-pCPT-cGMPS, an inhibitor of protein kinase G (PKG). Ca(2+) oscillations in myocytes and pericytes were also effectively blocked by NO donor SNAP. An Inhibitory effect of SNAP was markedly enhanced by zaprinast, a selective inh...Continue Reading
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