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Fig. 4. Modulation of CORM-2-induced suppression of ANP secretion (A), APP (B), ECF translocation (C) and ANP concentration (D) by several modulators. Twenty minutes before sample collection, atria were pretreated with KATP channel activator (pinacidil, 50 µM), mitochondrial KATP channel blocker (5-hydroxydecanoic acid; 5-HD, 100 µM), L-type Ca2+ channel blocker (diltiazem; Dilt, 50 µM), high-conductance Ca2+-activated K+ channel blocker (paxillin, 25 µM), nitric oxide synthase inhibitor (L-NAME; 100 µM), PI3K inhibitor (wortmannin; Wort, 10 µM) (LY-294002; LY, 10 µM), and soluble guanylate cyclase inhibitor (ODQ, 100 µM) or vehicle was perfused into atria after 10-min control period. Relative percent changes in atrial parameters by CORM-2 and vehicle in the presence of modulators are shown. CORM, carbon monoxide releasing molecule; ANP, atrial natriuretic peptide; APP, atrial pulse pressure; ECF, extracellular fluid. Values are expressed as the means ± SEM. * vs. vehicle group, p < 0.05, **p < 0.01, *** p < 0.005.
Korean J Physiol Pharmacol 2022;26:125-133 https://doi.org/10.4196/kjpp.2022.26.2.125
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