Abstract

ABSTRACT Larval Ambystoma tigrinum (Green) were cannulated non-occlusively in the truncus arteriosus and allowed to recover for 20–24 h. They were then subjected to 24 h of hypercapnia in three groups : those adapted to tap water, 100 mmol l−1 NaCl or running distilled water. The animals in tap water displayed a 32% compensation for the respiratory acidosis in that [HCO3−] and strong ion difference (SID) were elevated to return pH back towards the control level. The animals in 100 mmol l−1 NaCl behaved similarly. However, the animals in running distilled water were unable to compensate by increasing either [HCO3−] or strong ion difference until NaCl was added to the medium. The clear requirement for NaCl in the medium of salamanders that are compensating for a respiratory acidosis led to measurements of Na+ and Cl− fluxes. The influx of Na+ increased by 123 % in animals immersed in NaCl and by 39% in animals in Na2SO4. The influx of Cl− decreased by over 50% in animals immersed in NaCl and by over 30% in those in choline chloride. The transcutaneous potential difference increased rapidly and reversibly during hypercapnia and the increase was blocked by propranolol. These data suggest that the cutaneous active transport of Na+ into the extracellular space is stimulated and that the active transport of Cl− is simultaneously inhibited during hypercapnia. Measurement of circulating interrenal steroids (RIA) revealed a clear increase in aldosterone concentration during hypercapnia and a possible accompanying increase in corticosterone. The results suggest that the compensatory response to hypercapnia in larval A. tigrinum involves alterations in cutaneous ion transport which increase the extracellular SID. These cutaneous responses may be under the shortterm control of catecholamines and under the long-term control of interrenal steroids.

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