Role of Endothelial [Ca2i in EDHFMediated Responses in Pathology

An increasing number of studies demonstrate potentiated EDHF-mediated responses following a variety of pathological conditions, including ischemia/reperfusion (I/R), hypercholesterolemia, and congestive heart failure. The mechanism by which this potentiation occurs remains largely unknown. However, in cerebral I/R, the potentiated EDHF-mediated dilations are accompanied by augmented endothelial [Ca2+] responses [12]. In this case, for a given agonist concentration, there was a greater increase in

Figure 4 Role of endothelial K+ channels in endothelial [Ca2+]i response. Summary of simultaneous measurements of diameter (A) and endothelial [Ca2+] (B) in response to UTP (10-7 to 10-5M). All experiments were performed in the presence of L-NAME and indomethacin. Responses to UTP were performed in the presence of L-NAME/indomethacin alone (control), with luminal 60 mM K+ (high K+, nonselective K+ channel inhibitor), and in the presence of charybdo-toxin/apamin (ChTx/Apa; combination blocks all KCa channels). Diameter responses for both high K+ and ChTx/Apa were significantly different compared with control (two-way repeated-measures ANOVA). *Individual differences (P < 0.05, Tukey's test). Reproduced with permission from Marrelli et al. (2003). Am. J. Physiol. Heart Circ. Physiol. 285, H1590-H1599.

Figure 4 Role of endothelial K+ channels in endothelial [Ca2+]i response. Summary of simultaneous measurements of diameter (A) and endothelial [Ca2+] (B) in response to UTP (10-7 to 10-5M). All experiments were performed in the presence of L-NAME and indomethacin. Responses to UTP were performed in the presence of L-NAME/indomethacin alone (control), with luminal 60 mM K+ (high K+, nonselective K+ channel inhibitor), and in the presence of charybdo-toxin/apamin (ChTx/Apa; combination blocks all KCa channels). Diameter responses for both high K+ and ChTx/Apa were significantly different compared with control (two-way repeated-measures ANOVA). *Individual differences (P < 0.05, Tukey's test). Reproduced with permission from Marrelli et al. (2003). Am. J. Physiol. Heart Circ. Physiol. 285, H1590-H1599.

endothelial [Ca2+]i in the I/R endothelium compared with control. It was speculated that the greater Ca2+ responses following I/R might have resulted from some dysfunction in endothelial Ca2+ handling. It remains to be determined if endothelial Ca2+ is similarly altered in other pathological situations in which EDHF-mediated responses are potentiated.

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