Figure 1
PGI2-evoked contraction in NOS-inhibited mesenteric resistance arteries and effect of EP3 antagonism. (A) Comparison of responses evoked by PGI2 in L-NAME-treated WKY and SHR vessels with or without the presence of the IP antagonist CAY10441 (1 μM; CAY). N = 5 for each; ** P < 0.01 vs. WKY; ^ P < 0.05 and ^^ P < 0.01 vs. SHR; ++ P < 0.01 vs. WKY/CAY. (B) Comparison of the control contraction evoked by PGI2 (CTL; 10 μM) in WKY or SHR vessels obtained with CAY with that additionally with the TP antagonist SQ29548 (10 μM; +SQ), that with SQ29548 and the EP1 antagonist SC19220 (10 μM; +SQ/SC), or that with SQ29548 and the EP3 antagonist L798106 (1 μM; +SQ/L). (C) Representative traces showing the control contraction evoked by PGI2 (10 μM) in SHR vessels obtained with CAY (top) and that the additionally with the TP antagonist SQ29548 (10 μM; bottom). (D) Summary of control responses evoked by PGE2 (0.1 μM) on the contraction evoked by PE (3 μM) in L-NAME and SQ29548-treated WKY and SHR vessels and those obtained additionally with SC19220 (+SC) or L798106 (1 μM;+SQ/L). In (B) and (D), n = 5 for each; ** P < 0.01 vs. CTL; ^^ P < 0.01 vs. WKY counterparts; ++ P < 0.01 vs. +SQ.
