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  • 1
    Electronic Resource
    Electronic Resource
    Immunoreactivity for nitric oxide synthase and endothelin in the coronary and basilar arteries of renal hypertensive rats (1997)
    Springer
    Cell & tissue research 288 (1997), S. 509-516 
    Details
    ISSN: 1432-0878
    Keywords: Key words: One kidney/one clip hypertension ; Nitric oxide synthase ; Endothelin ; Coronary artery ; Basilar artery ; Rat (Sprague Dawley)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. The ultrastructural localization of immunoreactivity to nitric oxide synthase (type-III and type-II) and endothelin-1 was examined by using pre-embedding peroxidase-antiperoxidase techniques in the coronary and cerebral basilar arteries in renal hypertensive rats. Renal hypertension was produced by excision of the right kidney and clipping of the left renal artery. Controls were normotensive sham-operated rats (right surgical nephrectomy; a clip inserted near the left renal artery). Both in controls and hypertensive rats, immunoreactivities for nitric oxide synthase-III and endothelin-1 were localized within subpopulations of endothelial cells. In addition, signs of translocation of nitric oxide synthase-III were noted from the cytoplasm to the Golgi complex in endothelial cells of the basilar artery of hypertensive animals. Neither controls nor hypertensive rats showed immunoreactivity for nitric oxide synthase-II. Preparations of the right coronary artery from hypertensive rats displayed fewer endothelial cells positive to nitric oxide synthase-III than in controls, although there were no significant changes in the distribution of endothelin-1-positive endothelial cells in the coronary artery of hypertensive rats. In contrast, the basilar artery from hypertensive rats displayed no changes in the percentage of endothelial cells immuno-positive either for nitric oxide synthase-III or for endothelin-1. In consequence, the ratio of nitric oxide synthase-III:endothelin-1 was reduced in the coronary but not in the basilar artery. Therefore, the nitric oxide/endothelin-1 system appears to play different roles in the coronary and cerebral circulations during renal hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410050836
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  • 2
    Electronic Resource
    Electronic Resource
    Bile acids reversible effects on small intestinal permeability (1990)
    Springer
    Digestive diseases and sciences 35 (1990), S. 801-808 
    Details
    ISSN: 1573-2568
    Keywords: bile salts ; intestinal permeability ; paracellular permeability ; tight junctions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To define the action of deconjugated bile acids on the small intestinal permeability in an in vitrosystem, we investigated the effects of chenodeoxycholic acid and ursodeoxycholic acid on the rate of transmural flux of lactulose in jejunal and ileal mucosa of rabbits, stripped of their muscle layers and mounted in Ussing chambers. In a series of experiments, tissue samples from small intestinal segments either exposed to bile acids or not also were examined by scanning and transmission electron microscopy to study the integrity of the tight junctions. Results show that chenodeoxycholate, starting at the concentration of 0.1 mM, enhanced in a doserelated manner the trans epithelial flux of lactulose in the ileum. Both chenodeoxycholate (0.5 mM) and ursodeoxycholate (0.5 mM) significantly increased mucosal permeability to lactulose in jejunum and ileum; the effect of chenodeoxycholate was also shown to be reversible, as it completely disappeared within 40 min after its withdrawal and it did not result in permanent changes of epithelial transport function. Finally, the tight junctions appeared loosened by the addition of 1 mM chenodeoxycholate, suggesting that this is the major site of the transient bile acid increase of small intestinal permeability to compounds such as lactulose, having a molecular radius wider than 0.5 nm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01536791
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    Paper (German National Licenses)
    Fulltext
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