Abstract
The automaticity of the pulmonary vein myocardium is known to be the major cause of atrial fibrillation. We examined the involvement of angiotensin II in the automatic activity of isolated guinea pig pulmonary vein preparations. In tissue preparations, application of angiotensin II induced an automatic contractile activity; this effect was mimicked by angiotensin I and blocked by losartan, but not by PD123,319 or carvedilol. In cardiomyocytes, application of angiotensin II induced an increase in the frequency of spontaneous Ca2+ sparks and the generation of Ca2+ transients; these effects were inhibited by losartan or xestospongin C. In tissue preparations, angiotensin II caused membrane potential oscillations, which lead to repetitive generation of action potentials. Angiotensin II increased the diastolic depolarization slope of the spontaneous or evoked action potentials. These effects of angiotensin II were inhibited by SEA0400. In tissue preparations showing spontaneous firing of action potentials, losartan, xestospongin C or SEA0400 decreased the slope of the diastolic depolarization and inhibited the firing of action potentials. In conclusion, in the guinea pig pulmonary vein myocardium, angiotensin II induces the generation of automatic activity through activation of the IP3 receptor and the Na+-Ca2+ exchanger.
Highlights
The pulmonary vein wall contains a myocardial layer connected to the left atrial myocardium which is capable of generating spontaneous or triggered action potentials [1,2,3]
The results indicated that angiotensin II enhances the automaticity of the pulmonary vein myocardium through activation of the IP3 receptor and enhancement of the Na+-Ca2+ exchanger
We have been studying the basic mechanisms of the automatic activity of the guinea pig pulmonary vein myocardium and reported the involvement of intracellular Ca2+ movements and the
Summary
The pulmonary vein wall contains a myocardial layer connected to the left atrial myocardium which is capable of generating spontaneous or triggered action potentials [1,2,3]. The pulmonary vein myocardium in general has a lower (less negative) resting membrane potential when compared to atrial myocardium, which reflects the lower density of the inwardly rectifying potassium currents in the pulmonary vein cardiomyocytes [13,14,15]. This allows the generation of diastolic depolarization and the firing of action potentials. Analysis of intracellular Ca2+ movements, as well as of sarcolemmal ion currents, is essential for the understanding of the automaticity of the pulmonary vein myocardium
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