Branchial expression and localization of SLC9A2 and SLC9A3 sodium/hydrogen exchangers and their possible role in acid–base regulation in freshwater rainbow trout (Oncorhynchus mykiss)

Abstract

SUMMARY-uptake and base excretion. Levels of mRNA for NHE2, the predominant isoform in the gill, were increased during 72 h of hypercapnic acidosis; NHE3 mRNA and protein levels were unaffected. Because plasma cortisol levels were increased during hypercapnia (from 35.3±9.4 to 100.1±30.9 ng ml -1 ), the effects of experimentally elevated cortisol levels on NHE expression were investigated. The elevation of plasma cortisol using intraperitoneal implants caused a significant increase in NHE2 mRNA expression without affecting NHE3 mRNA or protein abundance. Thus, we suggest that NHE2 contributes to acid-base regulation during hypercapnia owing to its transcriptional regulation by cortisol. The finding of NHE expression in PNA + MRCs is discussed with reference to current models of ionic and acid-base regulation in teleost fish.

Ion uptake and acid secretion in zebrafish (Danio rerio)

“…In this situation, PNA -and PNA + MR cells in rainbow trout gills appear to be analogues of zebrafish HR and NaR cells, respectively; however, things are not so simple. Recently, Perry's group reported the localization of NHE2/3 in PNA + MR cells and acid-stimulated expression of NHE2, and argued against the base secretion function of PNA + MR cells in the current model (Ivanis et al, 2008). Moreover, it is worth noting a recent ISH and ICC study by the same group which reported that rainbow trout gills contain four populations of cells: (1) ECaC positive, (2) NKA positive, (3) ECaC and NKA positive, and (4) ECaC and NKA negative, confirming the broad distribution of ECaC among PNA -and PNA + MR cells as well as pavement cells.…”

“…However, it is notable that the situation may be species specific. In rainbow trout gills, NHE2 and H + -ATPase are respectively expressed in PNA + and PNA -cells (Ivanis et al, 2008), and hypercapnia treatment was found to upregulate the expression of the two transporters in the respective cells (Galvez et al, 2002;Ivanis et al, 2008).…”

“…In a recent review, Parks and colleagues (Parks et al, 2008) emphasized the thermodynamic constraints that prevent electroneutral apical NHE from functioning in most FW environments, thus favouring the applicability of ENaC-like channels to fish Na + -uptake mechanisms. Interestingly, Perry and colleagues (Ivanis et al, 2008) recently used double ISH and/or ICC to colocalize the mRNA and protein of both NHE2 and -3 in PNA + MR cells in gill sections of rainbow trout. This evidence appears to be against the argument of Goss's group, as described above, of the unfavourable operation of NHE in isolated trout gill cells (Parks et al, 2007;Parks et al, 2008).…”

Ammonia excretion in the freshwater planarianSchmidtea mediterranea

“…There is an open debate whether an electroneutral NHE that is driven only by the prevailing cation concentrations but not the electrical potential across the apical membrane could function in freshwater environments, as there is a potential threat of Na + loss (Orlowski and Grinstein, 2004;Parks et al, 2008). However, as mentioned above, there is recent evidence for the participation of an apically localized nhe3b in ammonia excretion in zebrafish larvae (Shih et al, 2012;Yan et al, 2007) and the presence of NHE2 and NHE3 in branchial Na + /K + -ATPase-positive peanut lectin agglutinin (PNA)-positive mitochondria-rich cells in rainbow trout (Ivanis et al, 2008). Moreover, there are precedents for electrogenic sodium:proton exchangers (i.e.…”

Rh glycoprotein expression is modulated in pufferfish (Takifugu rubripes) during high environmental ammonia exposure

“…Some or all of this may be facilitated by Rh proteins with pillar cell Rhag working in cooperation with basolateral Rhbg and apical Rhcg2 in the PVCs to facilitate ammonia efflux out of the gill. Additional support from the MRCs was suggested by Nakada et al (Nakada et al, 2007) as an auxiliary route of excretion via the basolateral Na Nawata and others al., 2008;Inokuchi et al, 2009;Ivanis et al, 2008;Yan et al, 2007), suggesting that the colocalisation of these transporters with Rhcg1 and NKA may serve to regulate ammonia excretion in a coordinated fashion from the MRCs. Additional mechanisms to reduce the entry or back flux of ammonia from the external water (downregulation of Rhag in pillar cells, and Rhbg in PVCs) are also suggested from the present study.…”