Although neural modulation of heart rate is well established among chordate animals, the Pacific hagfish (Eptatretus stoutii) lacks any cardiac innervation, yet it can increase its heart rate from the steady, depressed heart rate seen in prolonged anoxia to almost double its normal normoxic heart rate, an almost fourfold overall change during the 1-h recovery from anoxia. The present study sought mechanistic explanations for these regulatory changes in heart rate. We provide evidence for a bicarbonate-activated, soluble adenylyl cyclase (sAC)-dependent mechanism to control heart rate, a mechanism never previously implicated in chordate cardiac control.
Composite of 70 images showing sAC in the sinus venosus from a larger hagfish; the boxed areas are shown at higher magnification in i–v. In the higher-magnification images, the left panels are differential interference contrast, and the scale bars represent 50 µm. sAC immunostaining is in red; nuclei are stained in blue.