Effects of salinity on intestinal bicarbonate secretion and compensatory regulation of acid-base balance in Opsanus beta
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Published on: August 16, 2018
Janet Genz1, Josi R Taylor, Martin Grosell
1University of Miami, Rosenstiel School of Marine & Atmospheric Science, 4600 Rickenbacker Causeway, Miami, FL 33419-1098, USA. jgenz@rsmas.miami.edu
Abstract:
Marine teleosts have extracellular fluids less concentrated than their environment, resulting in continual water loss, which is compensated for by drinking, with intestinal water absorption driven by NaCl uptake. Absorption of Cl(-) occurs in part by apical Cl(-)/HCO(3)(-) exchange, with HCO(3)(-) provided by transepithelial transport and/or by carbonic anhydrase-mediated hydration of endogenous epithelial CO(2). Hydration of CO(2) also liberates H(+), which is transported across the basolateral membrane. In this study, gulf toadfish (Opsanus beta) were acclimated to 9, 35 and 50 ppt. Intestinal HCO(3)(-) secretion, water and salt absorption, and the ensuing effects on acid-base balance were examined. Rectal fluid excretion greatly increased with increasing salinity from 0.17+/-0.05 ml kg(-1) h(-1) in 9 ppt to 0.70+/-0.19 ml kg(-1) h(-1) in 35 ppt and 1.46+/-0.22 ml kg(-1) h(-1) in 50 ppt. Rectal fluid composition and excretion rates allowed for estimation of drinking rates, which increased with salinity from 1.38+/-0.30 to 2.60+/-0.92 and 3.82+/-0.58 ml kg(-1) h(-1) in 9, 35 and 50 ppt, respectively. By contrast, the fraction of imbibed water absorbed decreased from 85.9+/-3.8% in 9 ppt to 68.8+/-3.2% in 35 ppt and 61.4+/-1.0% in 50 ppt. Despite large changes in rectal base excretion from 9.3+/-2.7 to 68.2+/-20.4 and 193.2+/-64.9 mumol kg(-1) h(-1) in 9, 35 and 50 ppt, respectively, acute or prolonged exposure to altered salinities was associated with only modest acid-base balance disturbances. Extra-intestinal, presumably branchial, net acid excretion increased with salinity (62.0+/-21.0, 229.7+/-38.5 and 403.1+/-32.9 mumol kg(-1) h(-1) at 9, 35 and 50 ppt, respectively), demonstrating a compensatory response to altered intestinal base secretion associated with osmoregulatory demand.
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