Nitric oxide rectifies acid–base disturbance and modifies thyroid hormone activity during net confinement of air-breathing fish (Anabas testudineus Bloch)

Abstract

Nitric oxide (NO), a short-lived freely diffusible radical gas that acts as an important biological signal, regulates an impressive spectrum of physiological functions in vertebrates including fishes. The action of NO, however, on thyroid hormone status and its role in the integration of acid–base, osmotic and metabolic balances during stress are not yet delineated in fish. Sodium nitroprusside (SNP), a NO donor, was employed in the present study to investigate the role of NO in the stressed air-breathing fish Anabas testudineus. Short-term SNP treatment (1mM; 30min) interacted negatively with thyroid axis, as evident in the fall of plasma thyroxine in both stressed and non-stressed fish. In contrast, the cortisol responsiveness to NO was negligible. SNP challenge produced systemic alkalosis, hypocapnia and hyperglycemia in non-stressed fish. Remarkable acid–base compensation was found in fish kept for 60min net confinement where a rise in blood pH and HCO3 content occurred with a reduction in PCO2 content. SNP challenge in these fish, on the contrary, produced a rise in oxygen load together with hypocapnia but without an effect on HCO3 content, indicating a modulator role of NO in respiratory gas transport during stress response. SNP treatment reduced Na+, K+ ATPase activity in the gill, intestine and liver of both stressed and non-stressed fish, and this suggests that stress state has little effect on the NO-driven osmotic competence of these organs. On the other hand, a modulatory effect of NO was found in the kidney which showed a differential response to SNP, emphasizing a key role of NO in kidney ion transport and its sensitivity to stressful condition. H+-ATPase activity, an index of H+ secretion, downregulated in all the organs of both non-stressed and stressed fish except in the gill of non-stressed fish and this supports a role for NO in promoting alkalosis. The data indicate that, (1) NO interacts antagonistically with T4, (2) modifies respiratory gas transport and (3) integrates acid–base and osmotic actions during stress response in air-breathing fish. Collectively, this first evidence in fish indicate that NO can promote compensatory physiologic modification and that can reduce the magnitude of stress-induced acid–base and osmotic disturbance and that suggests a role for NO in the ease and ease response of this fish.