Nitric Oxide Modifies Hepatic and Cardiac Proton Gradient during Immersion-Stress in the Air- Breathing Fish (Anabas testudineus Bloch): Role of H+-ATPase and H+/K+-ATPase

Fishes have evolved complex and multi-step physiological mechanisms to drive ion homeostasis in challenging environments. Induction of stress that disturbs ion homeostasis in fishes evokes recovery response for their survival. Nitric Oxide (NO) as gasotransmitter modulates many physiological mechanisms including ion transport in osmoregulatory epithelia in teleosts. However, little is known about the role of NO in the transport of H⁺ ions that creates proton gradient with the help of H⁺-dependent ATPases like H⁺-ATPase and H⁺/K⁺-ATPase, particularly in hepatic and cardiac tissues of bony fish. We, thus, quantified H⁺-ATPase and H⁺/K⁺-ATPase in these tissues after in vivo treatments of NO donor, Sodium Nitro-Prusside (SNP) or NOS inhibitor, L-NAME, in both non-stressed and immersion-stressed air-breathing fish, Anabas testudineus Bloch. We found that elevated NO availability by SNP treatment lowered H⁺-ATPase-driven H⁺ transport in both hepatic and cardiac tissues of immersion-stressed fish. In contrast, NO depletion by L-NAME treatment elevated H⁺-ATPase activity in these tissues of stressed fish, pointing to a direct role of H⁺-ATPase in NO-mediated proton gradient regulation during stress condition. H⁺/K⁺-ATPase that drives H⁺ transport against K⁺ reduced its activity in cardiac tissue by SNP and L-NAME treatments. But L-NAME treatment in stressed fish imposed a higher H⁺ transport in cardiac tissue of these fish. Overall, the data indicate that NO has a vital role in the regulation of H⁺-ATPase-driven proton gradient in both cardiac and hepatic tissues of immersion-stressed fish.