Branchial Ammonia Excretion Research Articles

Ion Flux Rates, Acid–Base Status, and Blood Gases in Rainbow Trout,Salmo gairdneri, Exposed to Toxic Zinc in Natural Soft Water

Exposure to 0.8 mg Zn2+/L in natural soft water for up to 72 h was toxic to rainbow trout, Salmo gairdneri, causing an acid–base disturbance and net branchial ion losses. Mean arterial pH fell from 7.78 to 7.58. Both [Formula: see text] and lactate rose, indicating a mixed respiratory and metabolic acidosis, despite maintenance of high [Formula: see text] Net branchial uptake of Na+and Cl−became a net loss immediately following exposure to Zn2+, and this continued during 60 h of exposure. Net K+loss was exacerbated, and net Ca2+uptake was abolished. Unidirectional flux measurements with22Na+and36Cl−indicated an increased efflux immediately following zinc exposure. Both influx and efflux of Na+and Cl−were stimulated after 48–60 h in Zn2+. Both net branchial ammonia excretion and net branchial uptake of acidic equivalents from the water (=base loss) were greatly stimulated, the latter contributing to metabolic acidosis. Kidney function, as measured by urine flow rate and excretion of ammonia, acidic equivalents, Na+, Cl−, K+, and Zn2+, was relatively insensitive to the effects of zinc. The only renal component to be affected was Ca2+excretion, which decreased during a single flux period, possibly in response to the reduced entry of Ca2+at the gill. We conclude that toxic concentrations of zinc are capable of altering gill function so as to cause ionoregulatory and acid–base disturbances without disturbance of [Formula: see text].

An Analysis of Branchial Ammonia Excretion in the Freshwater Rainbow Trout: Effects of Environmental Ph Change and Sodium Uptake Blockade

ABSTRACT Short-term treatments (3 h) designed to change the relative NH3 and NH4+ (ΔNH4+) gradients and sodium transport (JNa) across the gills were employed to analyse the normal mechanism(s) of branchial ammonia excretion in trout acclimated to fresh water of pH ≃8·0. Control occurred in the absence of, or against, an apparent gradient, while ΔNH4+ was positive. Severe acid exposure (pH = 4·06) raised and ΔNH4+, abolished , and reduced by 28%, while moderate acidity (pH = 6·64), which also elevated had no significant influence on and . Severe alkaline exposure (pH = 9·4) raised ΔNH4+, reduced to a very negative value, and decreased and by equ1molar amounts, representing 55% and 80% of control levels respectively. Moderate alkalinity (pH = 8·69) had similar effects on and , but reduced and by only ∼25%. The sodium transport inhibitor amiloride (10−4moll −1 in the external water, pH ≃8·0) had very similar effects to pH = 4·06 on both and , but did not alter or . The results discount the quantitative importance of NH4+ diffusion and favour a flexible combination of NH3 diffusion and Na+/NH4+ exchange as the major mechanisms of , with the latter dominating under the particular control conditions of the present study.

Effect of amiloride on sodium transport across body surfaces of freshwater animals.

Effect of amiloride on sodium transport across body surfaces of freshwater animals.

Gill blood flow and ammonia excretion in the marine teleost, Myoxocephalus scorpius

1. 1. A method was developed to measure gill blood flow while quantitative evaluations of branchial ammonia excretion were being made. Gill blood flow was determined with oxygen by application of the Fick Principle, and the average flow was found to be 1665 ml/kg hr (95 per cent confidence limits = 1283–2047 ml/kg hr). This value was used to estimate the contribution of ammonia preformed in the blood to total ammonia excreted by the gills. 2. 2. Extraction of ammonia from blood passing through the gills could account for approximately 60 per cent of the excreted ammonia. The remaining 40 per cent could be accounted for by the extraction of plasma α-amino acid-N. These results indicate that both blood ammonia and plasma amino acids are sources of ammonia excreted by the gills of the marine teleost, Myoxocephalus scorpius.