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  • Tissue resistance  (2)
  • Desalination  (1)
  • 1990-1994  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of comparative physiology 164 (1994), S. 47-54 
    ISSN: 1432-136X
    Keywords: Esophagus ; Desalination ; Coupled NaCl transport ; Water permeability ; Eel,Anguilla japonica
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract To characterize mechanisms of esophageal desalination, osmotic water permeability and ion fluxes were measured in the isolated esophagus of the seawater eel. The osmotic permeability coefficient in the seawater eel esophagus was 2·10-4 cm·s-1. This value was much lower than those in tight epithelial, although the eel esophagus is a leaky epithelium with a tissue resistance of 77 ohm·cm-2. When the esophagus was bathed in normal Ringer solutions on both sides no net ion and water fluxes were observed. However, when mucosal NaCl concentration was increased by a factor of 3, Na+ und Cl- ions were transferred from mucosa to serosa (desalination). If only Na+ or Cl- concentration in the mucosal fluid was increased by a factor of 3, net Na+ and Cl- fluxes were reduced to 30–40%, indicating that 60–70% of the net Na+ and Cl- fluxes are coupled mutually. The coupled NaCl transport seems to be effective in desalting the luminal high NaCl. The remaining 30–40% of the total Na+ and Cl- fluxes seems to be due to a simple diffusion, because these components are independent of each other and follow their electrochemical gradients, and also because these fluxes remain even after treatment with NaCN or ouabain. A half of the coupled NaCl transport could be explained by a Na+/H+−Cl-/HCO 3 - double exchanger on the apical membrane of the esophageal epithelium, because mucosal amiloride and 4.4′-diisothiocyanatostilbene-2,2′-disulphonic acid inhibited the net Na+ and Cl- fluxes by approximately 30%. The other half of the coupled NaCl transport, which follows their electrochemical gradients, still remains to be explained.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of comparative physiology 163 (1993), S. 64-69 
    ISSN: 1432-136X
    Keywords: Serotonin ; Methacholine ; Catecholamine ; α2-receptor ; Adrenalin ; Short-circuit current ; Tissue resistance ; Eel, Anguilla japonica
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Dose-response relationships of catecholamines on seawater eel intestinal ion transport were obtained; the potency order being (-)adrenalin〉(-)noradrenalin=clonidine〉(±)noradrenalin (racemic form of noradrenalin)〉(-)phenylephrine〉dopamine〉(±)isoproterenol, indicating that α2 are more potent than α1- or β-agonists. In addition, the effects of adrenalin were completely blocked by yohimbine (α2-antagonists) but not by prazosin (α1-antagonists) or propranolol (β-antagonist). These results indicate the existence of an α2-receptor in the seawater eel intestine. Adrenalin may activate the α2-receptor physiologically, since adrenalin is the most potent stimulant and is the predominant catecholamine in American eel plasma (Hathaway and Epple 1989). Presumably ion and water absorption across the seawater eel intestine will be maintained by adrenalin. From the structure and the action of various agents used in the present study, structure-activity relationships of catecholamines are considered: hydroxyl groups on the benzene ring (catechol) seem to be essential for the α2-action in the seawater eel intestine and the presence of OH and CH3 on β-carbon and amide, respectively, seems to potentiate the α2-action.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of comparative physiology 163 (1993), S. 59-63 
    ISSN: 1432-136X
    Keywords: Active Cl- transport ; Noradrenalin α-type receptor ; Acetylcholine ; Serotonin ; Tissue resistance ; Eel, Anguilla japonica
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract After inhibiting ion and water transport with 10-6 mol·l-1 serotonin and 10-6 mol·l-1 methacholine, a muscarinic agonist of acetylcholine, 10-5 mol·l-1 (±)noradrenaline restored the serosa-negative transepithelial potential difference and short-circuit current in a step-like manner, accompanied by an increase in water absorption across the seawater eel intestine. Such recovery by noradrenalin was not obtained after pretreatment with 10-7 mol·l-1 eel atrial natriuretic peptide. This means that the inhibitory mechanisms of serotonin and acetylcholine are different from those of atrial natriuretic peptide. Similarly, 10-7 mol·l-1 clonidine and guanabenz (α2-agonists) also reversed the inhibitory action of serotonin and methacholine, but 10-7 mol·l-1 phenylephrine (α1-agonists) and 10-7 mol·l-1 isoproterenol (β-agonist) did not antagonize serotonin and methacholine actions. Further, the enhancement by 10-5 mol·l-1 noradrenalin was blocked by 10-4 mol·l-1 yohimbine (α2-agonists) and 10-4 mol·l-1 prazosin (α1-agonists), but not by 10-4 mol·l-1 propranolol (β-antagonist). Although relatively high dosage is required to obtain a significant effect, and discrimination between α1- and α2- is not successful in the present study, these results suggest that noradrenalin acts on an α-type receptor. The α-type receptor may exist on the enterocytes, since the effects of noradrenalin are observed even in the presence of 10-6 mol·l-1 tetrodotoxin. Interestingly, the tissue resistance also increased in parallel with increase in the short-circuit current after treatment with noradrenalin in the posterior part of the seawater eel intestine.
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