AKC Seminar: Fish intestinal HCO3-secretion: From molecules to the oceanic inorganic carbon cycle

August Krogh Club Seminar

Professor Dr. Martin Grosell

University of Miami, USA.


Marine fish and turtles maintain an internal osmotic pressure of ~300 mOsm and are forced to ingest seawater to compensate for diffusive water loss to the surrounding seawater. Imbibed seawater is desalinized in the water-impermeable esophagus, resulting in intestinal fluids slightly hyperosmotic to the blood plasma. Hypertonic fluid absorption by the intestinal epithelium is driven by Na+ and Cl- absorption, with ~50% of Cl- absorption being attributable to anion exchange resulting in high luminal concentrations of HCO3- (up to 100 mM). This luminal HCO3- reacts with Ca2+ ingested with seawater to form CaCO3 precipitates in the intestinal lumen, a reaction that results in reductions of luminal osmotic pressure by as much as 100 mOsm. Further reductions in luminal osmotic pressure occur as H+ secreted by distal intestinal segments is titrated with luminal HCO3-, facilitating continued water absorption. Intestinal anion exchange is thus important for solute coupled as well as osmotic fluid absorption and is mediated by the apical a6 member of the SLC26 family of anion transporters, an electrogenic nHCO3-/Cl- exchanger. HCO3- for intestinal secretion comes from two sources: Hydration of endogenous CO2, catalyzed by  cytosolic carbonic anhydrase (CAc), and HCO3- imported across the basolateral membrane via the NBC1 member of the SLC4 family of anion transporters, the latter forming the rate limiting step for overall intestinal HCO3- secretion rates. The formation of CaCO3 precipitates in the intestinal lumen appears to be facilitated by matrix proteins and the release of these CaCO3 precipitates to the environment may be mediated by a diuretic response in the distal intestinal segments. The distal intestine of marine fish responds to peptides of the guanylin family with a transient reversal of an absorptive to a secretory Cl- current mediated by NKCC1 and CFTR, a response which is associated with a secretory water flux. It is clear that the reduction in luminal osmotic pressure achieved by CaCO3 production is critical for osmoregulation and thus survival of marine organisms. The excretion of these precipitates also contributes significantly to the inorganic oceanic carbon cycle and likely explains observations of increased titratable alkalinity with depth above the aragonite lysocline (Ω=1), a connection that links fish physiology to important global processes.

Key publications for the talk

Esbaugh AJ, Mager EM, Brix KV, Santore R and Grosell M. 2013. Implications of pH manipulation methods for metal toxicity: Not all acidic environments are created equal. AQUATIC TOXICOLOGY 130: 27-30.

Grosell M. 2011. Intestinal anion exchange in marine teleosts is involved in osmoregulation and contributes to the oceanic inorganic carbon cycle. ACTA PHYSIOLOGICA  202: 421-434.

Wilson RW, Millero FJ, Taylor JR,  Walsh PJ, Christensen V, Jennings S and Grosell M. 2009. Contribution of Fish to the Marine Inorganic Carbon Cycle. SCIENCE 323: 359-36.

Research profile

Prof. Dr. Grosell is a comparative physiologist with extensive knowledge within the fields of aquatic toxicology as well as osmoregulation and acid-base balance in fish, the former including investigations into the toxicity of metals and crude oil to aquatic vertebrates as well as invertebrates. Research in Dr. Grosell's laboratory involves whole animal studies, biochemical and electrophysiological studies on isolated tissues and organs as well as molecular and isotope techniques.


20 May 2014

14:00-15:00: Seminar and discussion
15:00-15:30: Post seminar servings and socializing


Auditorium 1, August Krogh Building, Universitetsparken 13, DK-2100 Copenhagen


Participation is free, but please register here.

For PhD students

PhD students participating in August Krogh seminars receive 0,2 ECTS per seminar


Christian Frøsig, CFrosig@nexs.ku.dk, mobile +45 2875 1617

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