Fig. 1. (A) Effects of 2-chloro-N⁶-(3-iodobenzyl) adenosine-5′-N-methyluronamide (2-CI-IB-MECA) on pulse pressure (a), ECF translocation (b), ANP secretion (c), ANP concentration (d), and cAMP level (e) in isolated perfused beating rat atria. (B) Relative percent changes in atrial parameters using various concentrations of 2-CI-IB-MECA. Values are expressed as percent changes between the five control values and the last five experimental values exposed to 2-CI-IB-MECA from (A). Arrow indicates the start time of 2-CI-IB-MECA infusion. ECF transloc, ECF translocation; ANP conc, ANP concentration; *P < 0.05, **P < 0.01, ***P < 0.005 vs. corresponding group.

Fig. 2. Modification of the effects of A₃ agonists on pulse pressure, ECF translocation, ANP secretion, ANP concentration, and cAMP level in the presence of various receptor antagonists. The receptor antagonist was administered 40 min after the start of the perfusion and then, 2-CI-IB-MECA (30 μM) (A), 2-(1-hexylnyl)-N-methyladenosine (HEMADO, 100 μM) (B) or N⁶-(3-iodobenzyl) adenosine-5’-N-methyluronamide (IB-MECA, 100 μM) (C) was simultaneously infused after a 10-min control, collection period. The antagonists were MRS 1220 (MRS, 1 μM), ZM 241385 (ZM, 0.1 μM), and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 0.1 μM). Cont, agonist only, perfused group in the absence of a receptor antagonist. Legends are the same as in Fig. 1. *P < 0.05, **P < 0.01, ***P < 0.005 vs. control group.

Fig. 3. (A) Effects of 2-chloro-N⁶-(3-iodobenzyl) adenosine-5′-N-methyluronamide (2-CI-IB-MECA) on pulse pressure (a), ECF translocation (b), ANP secretion (c), ANP concentration (d), and cAMP level (e) in the presence of Ca²⁺ modulators. (B) Relative percent changes in atrial parameters by 2-CI-IB-MECA in the presence of Ca²⁺ modulators. The Ca²⁺ modulators were administered 40 min after the start of the perfusion for 60 min and then 2-CI-IB-MECA (30 μM) was simultaneously infused after a 10-min control collection period. As a control experiment, the Ca²⁺ modulator was administered 40 min after the start of perfusion for 60 min and perfusate was collected without 2-CI-IB-MECA. The modulators were ryanodine (Rya, 10 nM), thapsgargin (Thap, 1 μM) or trifluoroperazine (TFP, 50 μM), and nifedipine (Nife, 1 μM). 2-Cl-IB-MECA, 2-CI-IB-MECA only perfused groups in the absence of modulator. Legends are the same as in Fig. 1. *P < 0.05, **P < 0.01 vs. 2-CI-IB-MECA group; ^#P < 0.05, ^##P < 0.01 vs. corresponding group.

Fig. 4. Modification of the effects of 2-CI-IB-MECA on pulse pressure (A), ECF translocation (B), ANP secretion (C), and cAMP level (D) in the presence of the signal-transduction modulator. The modulator was administered 40 min after the start of the perfusion for 60 min and then 2-CI-IB-MECA (30 μM) was simultaneously infused after a 10-min control collection period, as described in Fig. 2. As a control experiment, the modulator was administered 40 min after the start of the perfusion for 60 min and the perfusate was collected without 2-CI-IB-MECA. The modulators were MDL-12330A (MDL, 5 μM) U-73122 (1 μM), 2-APB (1 μM). Legends are the same as in Fig. 1. *P < 0.05, **P < 0.01 vs. control group.