We use primary cultures of gill cells to illuminate if coordination between two types of acid-base sensors and their downstream effector protein PKA enables differential glycogen and mitochondrial mobilization during similar (but fundamentally different) types of acid-base stress. Along with increasing our understanding of these fundamental mechanisms that regulate cell physiology, this research is also relevant to human health and diseases of the kidney (e.g. chronic kidney disease) because the mechanisms responsible for acid-base regulation are evolutionarily conserved between our study system (ray gill cells) and mammalian kidney cells. This research has established ray gill cells as a viable non-model system to study essential cellular mechanisms related to acid-base regulation in both fish and mammals.