Atrial arrhythmias, including atrial fibrillation (AF), are a major mortality risk and a leading cause of stroke. Current pharmacological treatments for AF are poorly tolerated and may increase the risk of fatal ventricular arrhythmias. The IP3 signalling pathway has been proposed as an atrial specific target for AF therapy, and our work has demonstrated a link between atrial IP3 signalling and activation of calcium sensitive adenylyl cyclases AC1 and AC8 [1]. Here we demonstrate that a selective inhibitor of AC1, ST034307 [2], inhibits changes in chronotropy, but not inotropy, induced by activation of the IP3 pathway by the α-adrenoceptor agonist phenylephrine (PE). Experiments were carried out in accordance with the Animals (Scientific Procedures) Act 1986.  Data are presented as mean ± SEM. Whole left, and right mouse atria were mounted in organ baths containing 10ml physiological salt solution (PSS), maintained at 37°C with 95% O2 and 5% CO2 and connected to a mechanical force transducer. Spontaneous beating rate of right atria, and tension generated by left atria electrically paced at 5Hz, was recorded for the duration of experiments. Dose response curves were generated for PE (0.1-30μM) in the presence of 1μM metoprolol to inhibit beta-adrenergic signalling. PE increased beating rate of right atria with an increase of 12.1 ± 1.61% observed at 30μM (n=12). In the presence of 1μM ST034307, this increase was reduced (an increase of 7.43 ± 1.44% at 30μM; n=10, P 0.05). Further experiments were performed using isolated guinea pig atrial cells loaded with Fluo-5F-AM to record changes in calcium transient amplitude (CaT) generated by 10μM PE in the presence and absence of 1μM ST034307. Atrial myocytes were isolated from guinea pig hearts using enzymatic digestion and retrograde Langendorff perfusion (n=7). Cells were loaded with Fluo-5F-AM, perfused with PSS at 35 ± 2°C and field stimulated at 1Hz. CaTs were recorded and imaged using an inverted spinning disk confocal microscope connected to an EMCCD camera (iXON 897). 10μM PE induced a 35% increase in CaT from 3.56 ± 0.84 to 4.84 ± 1.04 (n=6, P < 0.05, paired t-test). In the presence of 1μM ST034307, CaT increased by 39% from 1.94 ± 0.34 to 2.69 ± 0.36 (n=15, P < 0.05, paired t-test), indicating that ST034307 does not inhibit the increase in CaT in response to PE. These results demonstrate AC1 is involved in the response of atrial pacemaker activity to α-adrenoreceptor stimulation, likely as a result of regulation of pacemaker currents within the sino-atrial node, and downstream of IP3 receptor activation. Conversely, AC1 activation does not appear to be involved in the inotropic response of atrial cells at either the whole-tissue or cellular level. These data support further investigation of cardiac AC1 as a potential pharmacological target for the treatment of atrial arrhythmias.