Small caliber arterial endothelial cells @entity460 signals elicited by XXXX are preserved from endothelial dysfunction.

@entity671 @entity19 @entity15395 @entity3739 @entity12845 @entity1617 @entity23451 @entity842 @entity460 @entity972 @entity141 @entity934
Endothelial cell (EC)-dependent vasodilation by @entity23451 ( @entity23451 ) is preserved in small caliber arteries in disease states where vasodilation by muscarinic receptors is decreased. In this study, we identified and characterized the @entity23451 -mediated intracellular @entity460 ( @entity141 )-release mechanisms in EC from small caliber arteries in healthy and diseased states. Mesenteric arterial EC were isolated from @entity23451 wild-type (WT) and null @entity19 , after saline (controls) or @entity15395 ( @entity15395 ) infusion, for imaging intracellular @entity460 and characterizing the @entity460 -release system by immunofluorescence. EC @entity141 signals comprised two forms of @entity141 -release events that had distinct spatial-temporal properties and occurred near either the plasmalemma (peripheral) or center of EC. In healthy EC, @entity23451 -dependent increases in the densities and firing rates of both forms of @entity141 -release were abolished by @entity671 receptor ( @entity12845 ) inhibitor, but partially reduced by transient potential vanilloid channels inhibitor @entity3739 red (RR). @entity934 ( @entity1617 )-induced less overall @entity141 -release than @entity23451 activation, but enhanced selectively the incidence of central events. @entity23451 -dependent @entity141 -activity, inhibitors sensitivities, @entity12845 , small- and intermediate-conductance @entity141 -activated @entity972 channels expressions were unchanged in EC from @entity15395 WT. However, the same cells exhibited decreases in @entity1617 -induced @entity141 -release, RR sensitivity, and endothelial @entity842 synthase expression, indicating @entity15395 -induced dysfunction was differentiated by receptor, @entity141 -release, and downstream targets of EC activation. We conclude that @entity23451 and muscarinic receptors selectively elicit two elementary @entity141 signals in single EC. @entity23451 -selective @entity12845 -dependent peripheral @entity141 -release mechanisms are identical between healthy and diseased states. Further study of @entity23451 -selective @entity141 -release for eliciting pathological and/or normal EC functions is warranted.
