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. Author manuscript; available in PMC: 2017 Jun 15.
Published in final edited form as: Mol Pharmacol. 1997 Sep;52(3):491–498. doi: 10.1124/mol.52.3.491

Fig. 7.

Fig. 7

Time course of the effects of CPA, m-DITC-ADAC, and A1-AdoR antagonist CPT on SH interval of guinea pig isolated, perfused hearts. Hearts were paced at an atrial cycle length of 300 msec throughout an experiment. A, CPA (50 nM) maximally and reversibly prolonged the SH interval. This effect was rapidly and nearly completely reversed by its washout or by the antagonist CPT (5 μM). Points, averages of SH interval determinations from two hearts. B, Lack of reversibility of m-DITC-ADAC (5 μM, 20 min)-induced SH interval prolongation. m-DITC-ADAC (5 μM) added to the perfusate increased the SH interval and caused second-degree AV block. After a 40-min washout, 1:1 AV conduction resumed, but the SH interval remained prolonged (79 ± 2 msec). A supramaximal concentration of CPT (5 μM) caused only a small (p > 0.05) reversal of the effect of m-DITC-ADAC. Points, mean ± standard error of responses of four hearts.