scholarly journals Vasodilation of swimbladder vessels in the european eel (Anguilla anguilla) induced by vasoactive intestinal polypeptide, nitric oxide, adenosine and protons

1999 ◽  
Vol 202 (8) ◽  
pp. 1005-1013
Author(s):  
T. Schwerte ◽  
S. Holmgren ◽  
B. Pelster
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Vasoactive Intestinal Polypeptide ◽  
Gland Cell ◽  
Perfusion Pressure ◽  
Cell Metabolism ◽  
Anguilla Anguilla ◽  
European Eel ◽  
Gas Gland ◽  
Intestinal Polypeptide

The effects of β-adrenergic stimulation, vasoactive intestinal polypeptide (VIP), adenosine, the nitric oxide (NO)-releasing agent sodium nitroprusside and of metabolic end-products of gas gland cell metabolism on swimbladder blood flow were investigated using saline- or blood-perfused swimbladder preparations of the freshwater European eel Anguilla anguilla. While β-adrenergic vasodilation was not detectable, a bolus injection of adenosine (100 microl, 10(−)7 mol l-1) and application of VIP (10(−)7 mol kg-1) caused a significant decrease in perfusion pressure in saline-perfused swimbladder preparations. Immunohistochemical analysis revealed the presence of VIP-immunoreactive nerve fibres in the swimbladder artery and in the swimbladder vein (seawater-adapted eels were used for immunohistochemical studies). Application of sodium nitroprusside also elicited a small, but significant, decrease in perfusion pressure in saline-perfused swimbladder preparations, while preincubation of swimbladder tissue with N(ω)nitro-l-arginine, a non-selective inhibitor of nitric oxide synthase, significantly enhanced the flow-induced increase in perfusion pressure. Lactate, the major metabolic end-product of gas gland cell metabolism, had no effect on perfusion pressure. In contrast, an increase in proton concentration in both saline- and blood-perfused preparations induced a vasodilation, as indicated by a significant decrease in perfusion pressure. The results demonstrate that VIP, NO, adenosine and protons may induce a vasodilation of swimbladder blood vessels. None of these effects, however, compares in time span with the previously described immediate, short-lasting vasodilation of swimbladder vessels elicited by pulse stimulation of the vagus nerve.

Control of acid secretion in cultured gas gland cells of the European eel Anguilla anguilla

1996 ◽  
Vol 270 (3) ◽  
pp. R578-R584
Author(s):  
B. Pelster ◽  
L. Pott
Keyword(s):  
Acid Secretion ◽  
Primary Culture ◽  
Single Cells ◽  
Calf Serum ◽  
Anguilla Anguilla ◽  
Beta Agonist ◽  
European Eel ◽  
Adrenergic Stimulation ◽  
Gland Cells ◽  
Gas Gland

Single cells and cell clusters isolated from the swimbladder epithelium of the European eel Anguilla anguilla attached to collagen S-coated petri dishes and proliferated in a modified Dulbecco's modified Eagle's medium, supplemented with 0.5% fetal calf serum. At a temperature of 20-22 degrees C, the growing colonies reached confluence typically within 6-8 days. Activities of glycolytic and pentose phosphate shunt enzymes remained stable or increased only slightly during the first 10 days of primary culture. Incubated in a defined medium providing glucose as a fuel, gas gland cells in primary culture produced and released lactic acid. The rate of acid secretion of cultured gas gland cells measured with a cytosensor microphysiometer was not influenced by cholinergic stimulation. Similarly, the Ca2+ ionophore A-23187 had no effect. Adrenergic stimulation with epinephrine or the beta-agonist isoproterenol also did not increase the rate of acid secretion, indicating that in gas gland cells the metabolic activity cannot be stimulated via beta-adrenergic stimulation followed by an increase in adenosine 3',5'-cyclic monophosphate (cAMP). Artificially increasing the intracellular concentration of cAMP by incubation with forskolin or the cAMP analogue 8-(4-chlorophenylthio)-cAMP even resulted in a marked reduction in the rate of acid secretion. The results demonstrate that primary cell culture provides a useful means for the analysis of metabolic control and of ion transfer processes in swimbladder gas gland cells.

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