Figure 1. Possible explanations for stress-induced sinus dysfunction in mice mutant for either Popdc1 or Popdc2.

(A) Wild-type sinus node and atrium. The origin of electrical impulse activation shifts upon stimulation of the β-adrenergic receptor to the inferior part of the sinus node. An electrocardiogram with normal activation of the atria is also shown. Note that the PP interval is regular. (B) Sinus node and atrium from a mouse mutant for either Popdc1 or Popdc2. The origin of electrical impulse activation cannot shift to the inferior part of the sinus node, because this part is absent. Furthermore, the sinus node has reduced in size, which may cause exit block or failure of impulse formation. An electrocardiogram during sinus node exit block or failure of impulse formation is also shown. Note that failure of atrial activation leads to an increase in PP interval (a so-called sinus pause).