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AIM: To compare the effects of moxonidine (Mox), clonidine (Clo), agmatine (Agm), and xylazine (Xyl) on action potentials (AP) of the rabbit sinoatrial node (SAN) pacemaker cells and investigate the contribution of α-adrenoceptors to the cardiac electrophysiologic responses induced by the agonists. METHODS: Intracellular microelectrode technique was used to record AP in the rabbit SAN pacemaker cells. Vasoconstrictive responses to norepinephrine (NE), Mox, Clo, Agm and Xyl were observed in the thoracic aorta and ear vein isolated from rabbits. RESULTS: (1) In the rabbit thoracic aorta, a rank order of potency producing vasoconstrictive responses was NE>Clo>Mox; and a rank order of potency in ear vein was Clo>NE>Xyl=Mox. Agm did not produce any vascular responses in both preparations, and Xyl did not produce vascular responses in the thoracic aorta. (2) Mox, Clo, Xyl, and Agm concentration-dependently decreased the rate of pacemaker firing (RPF), and prolonged APD_(50) and APD_(90) in the rabbit SAN pac
AIM: To compare the effects of moxonidine (Mox), clonidine (Clo), agmatine (Agm), and xylazine (Xyl) on action potentials (AP) of the rabbit pacemaker cells and investigate the contribution of α- METHODS: Intracellular microelectrode technique was used to record AP in the rabbit SAN pacemaker cells. Vasoconstrictive responses to norepinephrine (NE), Mox, Clo, Agm and Xyl were observed in the thoracic aorta and ear vein from rabbits. RESULTS: (1) In the rabbit thoracic aorta, a rank order of potency producing vasoconstrictive responses was NE> Clo> Mox; and a rank order of potency in ear vein was Clo> NE> Xyl = Mox. Agm did not produce any vascular responses in both preparations, and Xyl did not produce vascular responses in the thoracic aorta. (2) Mox, Clo, Xyl, and Agm concentration-dependently decreased the rate of pacemaker firing (RPF), and prolonged APD_ (50) and APD_ (90) in the rabbit SAN pac