Regulation of cation transport by low doses of glucocorticoids in in vivo adrenalectomized rat colon.

Bastl, C. P.

doi:10.1172/jci113079

Cited by 29 publications

(12 citation statements)

References 55 publications

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“…20 Corticosteroids could affect Bruch membrane via their known inhibition of collagen synthesis. 152 Finally, epithelial water and ion transport are altered by corticosteroids, 16,72,182,197 and this might impair the barrier function of the RPE. Arndt and colleagues studied RPE tissue in vitro and showed that administration of hydrocortisone decreased the transepithelial membrane potential and resistence.…”

Section: Pathophysiologymentioning

confidence: 99%

Central Serous Chorioretinopathy: Update on Pathophysiology and Treatment

Nicholson

Noble

Forooghian

et al. 2013

Survey of Ophthalmology

561

573

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Recent technological advances have led to an improved understanding of central serous chorioretinopathy (CSC): new pathophysiological insights, new imaging techniques for diagnosis and management, and new treatments. The primary role of the choroid has become more widely accepted with widespread use of indocyanine green angiography. Optical coherence tomography (OCT), and particularly enhanced depth imaging OCT, demonstrate a thickened and engorged choroid. Adaptive optics, fundus autofluorescence, multifocal electroretinography, microperimetry, and contrast sensitivity testing reveal that patients with even a mild course suffer previously undetected anatomic and functional loss. While focal laser and photodynamic therapy are the current standard of care for persistent subretinal fluid in CSC, they are not appropriate in all cases, and the optimal timing of intervention remains unclear.

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Section: Pathophysiologymentioning

confidence: 99%

Central Serous Chorioretinopathy: Update on Pathophysiology and Treatment

Nicholson

Noble

Forooghian

et al. 2013

Survey of Ophthalmology

561

573

View full text Add to dashboard Cite

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“…There is abundant experimental evidence that adrenal corticosteroids increase and adrenalectomy decreases Na + transport and the permeability of the apical membrane of colonocytes to Na § [2,3,6,29,41]. The corticosteroids increase Na § flux into the cell which in turn stimulates the active Na + extrusion via the Na,K pump, because the intracellular Na + activity remains approximately constant in spite of the manifold variations of Na + current across the epithelium [38].…”

Section: Introductionmentioning

confidence: 99%

“…The curves were calculated using an equa-tion derived from Michaelis-Menten kinetics with three noninteracting Na + binding sites which gave better fit than the model of highly cooperative sites [17]. The noninteracting model equation was (2) where Isc was the value of the short-circuit current at various concentrations of Na +, 1 max the maximal SC value oflsc, KNa the substrate concentration at which 50% of binding sites were occupied and [Na § the mucosal Na + concentration. The K0.…”

mentioning

confidence: 99%

Na, K-ATPase and the development of Na+ transport in rat distal colon

et al. 1991

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Na,K-ATPase function was studied in order to evaluate the mechanism of increased colonic Na+ transport during early postnatal development. The maximum Na(+)-pumping activity that was represented by the equivalent short-circuit current after addition of nystatin (ISCN) did not change during postnatal life or after adrenalectomy performed in 16-day-old rats. ISCN was entirely inhibited by ouabain; the inhibitory constant was 0.1 mM in 10-day-old (young) and 0.4 mM in 90-day-old (adult) rats. The affinity of the Na,K pump for Na+ was higher in young (11 mM) than in adult animals (19 mM). The Na,K-ATPase activity (measured after unmasking of latent activity by treatment with sodium dodecylsulfate) increased during development and was also not influenced by adrenalectomy of 16-day-old rats. The inhibitory constant for ouabain (KI) was not changed during development (0.1-0.3 mM). Specific [3H]ouabain binding to isolated colonocytes increased during development (19 and 82 pmol/mg protein), the dissociation constant (KD) was 8 and 21 microM in young and adult rats, respectively. The Na+ turnover rate per single Na,K pump, which was calculated from ISCN and estimated density of binding sites per cm2 of tissue was 500 in adult and 6400 Na+/min.site in young rats. These data indicate that they very high Na+ transport during early postnatal life reflects an elevated turnover rate and increased affinity for Na+ of a single isoform of the Na,K pump. The development of Na+ extrusion across the basolateral membrane is not directly regulated by corticosteroids.

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“…DOCA treatment restored K-NPPase in adrenalectomized rats. The treatment with dexamethasone had a much smaller effect than with DOCA even though a dose of dexamethasone of 5 ~g per 100 g body wt per 12 h occupied more than 90% of distal colon glucocorticoid receptors and less than 30% of mineralocorticoid receptors, and a dose 0.5 lJg per 100 g body wt per 12 h occupied more than 60% of glucocorticoid and less than 10% of mineralocorticoid receptors (Bastl, 1987(Bastl, , 1988. Thus, mineralocorticoids seem to exert a decisive role in the regulation of colonic Na,K-ATPase, even if the possibility that glucocorticoids act through high-specificity glucocorticoid receptors cannot be excluded.…”

Section: Discussionmentioning

confidence: 90%

Corticosteroid induction of renal and intestinal K+-dependentp-nitrophenylphosphatase in young and adult rats

Zemanová

Pácha

1996

Histochem J

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The post-natal development of the K(+)-dependent p-nitrophenylphosphatase (K-NPPase) activity of the Na, K-ATPase complex and its regulation by corticosteroids was studied in renal and intestinal epithelia of the rat using the p-nitrophenylphosphatecerium capture method. The distribution of the phosphatase was analysed in detail in the renal epithelia of the medullary thick ascending limb of Henle's loop and distal convoluted tubule and in the surface epithelial cells of the distal colon. The convoluted tubule and Henle's loop segments showed a stronger reaction for K-NPPase than the colon epithelium both in adult and young animals (suckling and weanling pups). The intensity of staining rose progressively in all three epithelia during early postnatal development and reached the highest levels during the weaning period and in adulthood. The most distinct change was observed between days 10 and 16. Adrenalectomy significantly reduced the density of the final reaction product in weanling and adult rats. Replacement hormone therapy of adrenalectomized weanling rats with the glucocorticoid dexamethasone restored the K-NPPase activity in the two renal epithelia, whereas the mineralocorticoid deoxycorticosterone acetate had no effect on the activity in the medullary thick ascending limb, a very slight effect in distal convoluted tubules, and a strong effect on the distal colon epithelial activity. The observed small effect of the mineralocorticoid in distal convoluted tubule activity may reflect a cross-over into glucocorticoid receptors. We conclude that the postnatal development of Na, K-ATPase is regulated by glucocorticoids in nephron epithelia and predominantly by mineralocorticoids in the surface enterocytes of the distal colon.

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Regulation of cation transport by low doses of glucocorticoids in in vivo adrenalectomized rat colon.

Cited by 29 publications

References 55 publications

Central Serous Chorioretinopathy: Update on Pathophysiology and Treatment

Central Serous Chorioretinopathy: Update on Pathophysiology and Treatment

Na, K-ATPase and the development of Na+ transport in rat distal colon

Corticosteroid induction of renal and intestinal K+-dependentp-nitrophenylphosphatase in young and adult rats

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