The alkaline tide and ammonia excretion after voluntary feeding in freshwater rainbow trout

Abstract

SUMMARYWe investigated the potential acid-base and nitrogenous waste excretion challenges created by voluntary feeding in freshwater rainbow trout, with particular focus on the possible occurrence of an alkaline tide (a metabolic alkalosis created by gastric HCl secretion during digestion). Plasma metabolites (glucose, urea and ammonia) were measured at various time points before and after voluntary feeding to satiation (approximately 5% body mass meal of dry commercial pellets), as was the net flux of ammonia and titratable alkalinity to the water from unfed and fed fish. Arterial blood, sampled by indwelling catheter, was examined for post-prandial effects on pH, plasma bicarbonate and plasma CO 2 tension. There was no significant change in plasma glucose or urea concentrations following feeding, whereas plasma ammonia transiently increased, peaking at threefold above resting values at 12 h after the meal and remaining elevated for 24 h. The increased plasma ammonia was correlated with an increase in net ammonia excretion to the water, with fed fish significantly elevating their net ammonia excretion two-to threefold between 12 and 48 h post feeding. These parameters did not change in unfed control fish. Fed fish likewise increased the net titratable base flux to the water by approximately threefold, which resulted in a transition from a small net acid flux seen in unfed fish to a large net base flux in fed fish. Over 48 h, this resulted in a net excretion of 13·867·μmol·kg -1 more base to the external water than in unfed fish. The arterial blood exhibited a corresponding rise in pH (between 6 and 12 h) and plasma bicarbonate (between 3 and 12 h) following feeding; however, no respiratory compensation was observed, as Pa CO 2 remained constant. Overall, there was evidence of numerous challenges created by feeding in a freshwater teleost fish, including the occurrence of an alkaline tide, and its compensation by excretion of base to the external water. The possible influence of feeding ecology and environmental salinity on these challenges, as well as discrepancies in the literature, are discussed.

Revisiting the effects of crowding and feeding in the gulf toadfish, Opsanus beta: the role of Rhesus glycoproteins in nitrogen metabolism and excretion

“…Under these circumstances, ammonia liberated from post-prandial catabolic processes would begin to accumulate in the plasma and eventually translate into elevated rates of ammonia excretion, as was the case in the present study. This pattern is also observed in other ammoniotelic teleosts following feeding (Kaushik and Teles, 1985;Kaushik and Gomes, 1988;Alsop and Wood, 1997;Wicks and Randall, 2002;Bucking and Wood, 2008;Bucking et al, 2009;Zimmer et al, 2010). In addition, this explanation also clarifies why the increases in plasma ammonia levels (Fig.1B) and ammonia excretion rates (Fig.1A) observed in crowded and unconfined fish during the post-prandial period were of similar magnitude.…”

“…Higher hepatic Rh mRNA expression was accompanied by an upregulation of both Rhcg1 and Rhcg2 at the gill (Fig.5A). This scenario is similar to that of most teleosts that simply excrete the majority of excess ammonia across the gills (Kaushik and Teles, 1985;Wicks and Randall, 2002;Bucking and Wood, 2008;Bucking et al, 2009). Indeed, physiological data from the present study confirmed that unconfined toadfish excreted the majority of their wastes as ammonia (Table2), and also had higher rates of ammonia excretion than their crowded counterparts.…”

“…We hypothesized that Rh glyoproteins contribute to toadfish ammonia excretion and, in particular, that unconfined (ammoniotelic) fish would exhibit higher gill Rh expression than crowded (ureotelic) individuals. Furthermore, as feeding is associated with increases in both plasma ammonia and ammonia excretion in ammoniotelic teleosts (Brett and Zala, 1975;Kaushik and Teles, 1985;Alsop and Wood, 1997;Wicks and Randall, 2002;Bucking and Wood, 2008) and has, more recently, been shown to induce Rhcg2 mRNA expression (Zimmer et al, 2010), we anticipated that feeding would differentially modulate Rh expression in the gill and along the gastrointestinal tract in unconfined and crowded toadfish.…”

Diet influences salinity preference of an estuarine fish, the killifishFundulus heteroclitus

“…acid-base regulation (Bucking et al, 2009;Taylor et al, 2007;Taylor and Grosell, 2006;Taylor and Grosell, 2009;Wood et al, 2010), salt balance (Bucking et al, 2011;Taylor et al, 2007;Taylor and Grosell, 2006)] and freshwater [e.g. acid-base regulation (Bucking and Wood, 2008;Cooper and Wilson, 2008;Taylor et al, 2007;Wood et al, 2010), salt balance (Bucking and Wood, 2006a;Bucking and Wood, 2007;Taylor et al, 2007), water balance (Bucking and Wood, 2006b)]. In general, feeding appears to result in salinity-dependent alterations in ion, water and acid-base transport processes in order to alleviate digestion-induced disruptions in homeostasis.…”

Ammonia sensing by neuroepithelial cells and ventilatory responses to ammonia in rainbow trout

“…Wicks and Randall, 2002;Bucking and Wood, 2008), exhaustive exercise (e.g. Wood, 1988;Wang et al, 1994) or exposure to high environmental ammonia (HEA) (Wilson and Taylor, 1992;Knoph, 1996;Nawata et al, 2007), suggesting the possible function of ammonia to induce hyperventilation in these circumstances.…”