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  • 1
    ISSN: 1432-2013
    Keywords: Enterocyte differentiation Intestinal transport Iron deficiency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Iron deficiency induced in rats maintained on a commercial diet with a low iron content has been used to investigate adaptive mechanisms that enhance duodenal iron uptake. These adaptive changes have been divided into those that result from changes in villus surface area (structural adaptation) and those that reflect changes in the way individual enterocytes express iron transport function (cellular adaptation). Cellular adaptation was assessed by carrying out microdensitometry of autoradiographs prepared from duodenal tissue previously incubated for 5 min in 200 µmol/l 59Fe2+-ascorbate. Structural adaptation was studied by performing image analysis of microdissected and sectioned villi. Cellular adaptation involved increased iron uptake by enterocytes present in the lower villus. Thus iron deficiency resulted in a threefold enhanced expression of uptake in the lower 100 µm villus (3.9±2.4 versus 12.6±1.5 arbitrary units, P〈0.001). Maximal uptake was reached in the upper region of both control and iron-deficient villi, but iron deficiency had no effect on cellular uptake at this part of the villus. Structural adaptation involved the lengthening (+16%, P〈0.05) and broadening (+14%) of villi in the duodenum of iron-deficient rats. The resultant expansion in villus area caused a further increase in uptake that was mostly expressed in the upper villus. Maximal uptake corrected for structure occurred in the middle third of villi from control and iron-deficient rats. Cellular plus structural adaptation produced a twofold increase in iron uptake. More than half of this effect was caused by changes in villus structure. [3H]Thymidine labelling experiments revealed a slightly earlier expression of enterocyte iron uptake in iron deficiency.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1434-0879
    Keywords: Key words Endothelin receptors ; Nitric oxide synthase ; Rabbit ; Bladder obstruction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bladder outlet obstruction (BOO) is associated with altered bladder structure and function. Endothelin-1 (ET-1) has mitogenic and potent contractile properties. There are two ET receptors: ETA and ETB. Nitric oxide synthase (NOS) is the enzyme responsible for the synthesis of nitric oxide (NO) which is involved in smooth muscle relaxation. We investigated whether there are any changes in the density of ET-receptors and NOS in the detrusor and bladder neck in a rabbit model of BOO. Partial BOO was induced in adult male New Zealand White rabbits. Sham operated age-matched rabbits acted as controls. After six weeks the urinary bladders were excised and detrusor and bladder neck sections incubated with radioligands for ET-1, ETA and ETB receptors and with [3H]–l-NOARG (a ligand for NOS). NADPH histochemistry was also performed. BOO bladder weights were significantly increased (P=0.002). ET-1 binding and ETA receptor binding sites were significantly increased in the BOO detrusor smooth muscle (P=0.04, P=0.03 respectively) and urothelium (P=0.002, P=0.02 respectively). ETB receptor binding sites were also significantly increased in the BOO detrusor smooth muscle (P=0.04). However, there was no change in the BOO bladder neck. NOS was significantly decreased in the detrusor smooth muscle (P=0.003) and urothelium (P=0.0002). In the bladder neck NOS was also significantly reduced in the urothelium (P=0.003). NADPH staining was decreased in the detrusor and bladder neck. The up-regulation of ET receptors along with the down-regulation of NOS in the detrusor may contribute to the symptoms associated with BOO. Since ET-1 has a mitogenic role, especially via its ETA receptors, the increase in ETA receptors may also be involved in detrusor hyperplasia and hypertrophy in BOO. ET antagonists may therefore have a role in the treatment of patients with BOO.
    Type of Medium: Electronic Resource
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