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Ventricular myocytes deficient in endothelial nitric oxide synthase (NOS3 −/− ) exhibit prolonged action potential (AP) duration and enhanced spontaneous activity (early and delayed afterdepolarizations) during   β  -adrenergic (  β  -AR) stimulation. Studies have shown that nitric oxide is able to regulate various K +  channels. Our objective was to examine if NOS3 −/−  myocytes had altered K +  currents. APs, transient outward ( I   to ), sustained ( I   Ksus ), and inward rectifier ( I   K1 ) K +  currents were measured in NOS3 −/−  and wild-type (WT) myocytes. During   β  -AR stimulation, AP duration (measured as 90% repolarization-APD 90 ) was prolonged in NOS3 −/−  compared to WT myocytes. Nevertheless, we did not observe differences in  I   to ,  I   Ksus , or  I   K1  between WT and NOS3 −/−  myocytes. Our previous work showed that NOS3 −/−  myocytes had a greater Ca 2+  influx via L-type Ca 2+  channels with   β  -AR stimulation. Thus, we measured   β  -AR-stimulated SR Ca 2+  load and found a greater increase in NOS3 −/−  versus WT myocytes. Hence, our data suggest that the prolonged AP in NOS3 −/−  myocytes is not due to changes in  I   to ,  I   Ksus , or  I   K1 . Furthermore, the increase in spontaneous activity in NOS3 −/−  myocytes may be due to a greater increase in SR Ca 2+  load. This may have important implications for heart failure patients, where arrhythmias are increased and NOS3 expression is decreased.

Prolonged Action Potential and After depolarizations Are Not due to Changes in Potassium Currents in NOS3 Knockout Ventricular Myocytes