This review focuses on the structure and function of the branchial chloride cell in freshwater fishes. The mitochondria-rich chloride cell is believed to be the principal site of trans-epithelial Ca2+ and Cl- influxes. Though currently debated, there is accruing evidence that the pavement cell is the site of Na+ uptake via channels linked electrically to an apical membrane vacuolar H(+)-ATPase (proton pump). Chloride cells perform an integral role in acid-base regulation. During conditions of alkalosis, the surface area of exposed chloride cells is increased, which serves to enhance base equivalent excretion as the rate of Cl-/HCO3- exchange is increased. Conversely, during acidosis, the chloride cell surface area is diminished by an expansion of the adjacent pavement cells. This response reduces the number of functional Cl-/HCO3- exchangers. Under certain conditions that challenge ion regulation, chloride cells proliferate on the lamellae. This response, while optimizing the Ca2+ and Cl- transport capacity of the gill, causes a thickening of the blood-to-water diffusion barrier and thus impedes respiratory gas transfer.

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In fish, the catecholamine hormones adrenaline and noradrenaline are released into the circulation, from chromaffin cells, during numerous 'stressful' situations. The physiological and biochemical actions of these hormones (the efferent adrenergic response) have been the focus of numerous investigations over the past several decades. However, until recently, few studies have examined aspects involved in controlling/modulating catecholamine storage and release in fish. This review provides a detailed account of the afferent limb of the adrenergic response in fish, from the biosynthesis of catecholamines to the exocytotic release of these hormones from the chromaffin cells. The emphasis is on three particular topics: (1) catecholamine biosynthesis and storage within the chromaffin cells including the different types of chromaffin cells and their varying arrangement amongst species; (2) situations eliciting the secretion of catecholamines (e.g. hypoxia, hypercapnia, chasing); (3) cholinergic and non-cholinergic (i.e. serotonin, adrenocorticotropic hormone, angiotensin, adenosine) control of catecholamine secretion. As such, this review will demonstrate that the control of catecholamine storage and release in fish chromaffin cells is a complex processes involving regulation via numerous hormones, neurotransmitters and second messenger systems.

In freshwater fishes, the gill and kidney are intricately involved in ionic and acid-base regulation owing to the presence of numerous ion channels, pumps, or exchangers. This review summarizes recent developments in branchial and renal ion transport physiology and presents several models that integrate epithelial ion and acid-base movements in freshwater fishes. At the gill, three cell types are potentially involved in ionic uptake: pavement cells, mitochondria-rich (MR) PNA(+) cells, and MR PNA(-) cells. The transfer of acidic or basic equivalents between the fish and its environment is accomplished largely by the gill and is appropriately regulated to correct acid-base imbalances. The kidney, while less important than the gill in overall acid or base excretion, has an essential role in regulating systemic acid-base balance by controlling HCO(3) (-) reabsorption from the filtrate.

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Braun MH, Steele SL, Ekker M, Perry SF. Nitrogen excretion in developing zebrafish (Danio rerio): a role for Rh proteins and urea transporters.

SummaryCarbonic anhydrase (CA) is the zinc metalloenzyme that catalyses the reversible reactions of CO 2 with water. CA plays a crucial role in systemic acid-base regulation in fish by providing acid-base equivalents for exchange with the environment. Unlike airbreathing vertebrates, which frequently utilize alterations of breathing (respiratory compensation) to regulate acid-base status, acid-base balance in fish relies almost entirely upon the direct exchange of acid-base equivalents with the environment (metabolic compensation). The gill is the critical site of metabolic compensation, with the kidney playing a supporting role. At the gill, cytosolic CA catalyses the hydration of CO 2 to H + and HCO 3 -for export to the water. In the kidney, cytosolic and membranebound CA isoforms have been implicated in HCO 3 -reabsorption and urine acidification. In this review, the CA isoforms that have been identified to date in fish will be discussed together with their tissue localizations and roles in systemic acid-base regulation.

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