Aldosterone: Its occurrence, metabolism and binding in the rabbit eye

Stárka, L.; Hampl, Richard; Gregorová, I; Obenberger, J

doi:10.1016/0014-4835(77)90249-4

Cited by 14 publications

(9 citation statements)

References 11 publications

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“…Our data and those of Starka et al [10] indicate that aldosterone and its receptors are present in the rabbit eye. Furthermore, our data suggests that mineralocorticoid receptors may constitute a significant portion of the total corticoid receptors in the eye.…”

Section: Discussionsupporting

confidence: 71%

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Mineralocorticoid Receptors in the Rabbit Iris-Ciliary Body

Schwartz¹,

Wysocki²

1997

Ophthalmic Res

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To demonstrate the presence of mineralocorticoid receptors, specifically aldosterone receptors, iris-ciliary body cytosol from New Zealand albino rabbits was incubated with increasing amounts (0.5–20.0 nM) of radiolabeled aldosterone in the presence and absence of a 100-fold excess of aldosterone. A glucocorticoid receptor blocker, RU-28362, was employed when various steroids were allowed to compete with aldosterone for binding sites on the aldosterone receptor. Aldosterone bound to two classes of receptor proteins. Scatchard analysis of the data indicated one component to bind aldosterone with high affinity (K_d = 2.2 × 10^––9M) and low capacity (B_max = 32 fmol/mg protein). If the concentration of aldosterone is increased, it also binds to a second component, but with a lower affinity (K_d = 9.8 × 10^––9M) and greater capacity (B_max = 64 fmol/mg protein).

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Section: Discussionsupporting

confidence: 71%

“…[10] identified aldosterone in the aqueous humor (63.5 pmol/1) and aldoste rone receptors in the iris-ciliary body of rab bits. This study also indicated some metabo lism of aldosterone by the detection and iden tification of aldosterone metabolites in the iris-ciliary body.…”

Section: Discussionmentioning

confidence: 99%

Mineralocorticoid Receptors in the Rabbit Iris-Ciliary Body

Schwartz¹,

Wysocki²

1997

Ophthalmic Res

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“…used in a variety of in vitro and in vivo experiments investigating both corneal pathophysiology (Becker 1961, Starka et al 1977, Green et al 1981, Usukura et al 1988, Felche & Sigler 2002, Nakamura et al 2003, Tungsiripat et al 2003, Ivarsen et al 2004, Mimura et al 2005 and IOP (Becker 1961, Starka et al 1977, Green et al 1981, Usukura et al 1988, Felche & Sigler 2002, Nakamura et al 2003, Tungsiripat et al 2003, Ivarsen et al 2004, Mimura et al 2005. Furthermore, our in-house generated polyclonal antibody to human 11b-HSD1 shared a 93% homology to the rabbit 11b-HSD1 amino acid sequence and the corticosteroid hormone profile is similar to humans (i.e.…”

Section: Western Blot Analysesmentioning

confidence: 90%

Characterisation of the prereceptor regulation of glucocorticoids in the anterior segment of the rabbit eye

Onyimba¹,

Vijapurapu²,

Curnow³

et al. 2006

Journal of Endocrinology

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The prereceptor regulation of glucocorticoids (GCs) by 11b-hydroxysteroid dehydrogenase type-1 (11b-HSD1), a bidirectional isozyme that interconverts active (cortisol) and inactive (cortisone) GCs, is an established determinant of GC function in tissues such as liver, adipose and bone. Although the therapeutic use of GCs is abundant in ophthalmic practice, where GC interactions with nuclear receptors modulate gene transcription, the prereceptor regulation of endogenous cortisol is not well described in ocular tissues. Recent descriptive studies have localised 11b-HSD1 to the human corneal epithelium and non-pigmented epithelium (NPE) of the ciliary body, indicating a link to corneal epithelial physiology and aqueous humour production. In this study, we characterise the functional aspects of the autocrine regulation of GCs in the anterior segment of the rabbit eye. Using our in-house generated primary antibody to human 11b-HSD1, immunohistochemical analyses were performed on paraffin-embedded sections of whole New Zealand white albino rabbits, (NZWAR) eyes. As in human studies, 11b-HSD1 was localised to the corneal epithelium and the NPE. No staining was seen in the albino 'pigmented' ciliary epithelium. Specific enzyme assays for oxo-reductase (cortisone/cortisol) and dehydrogenase (cortisol/cortisone) activity indicated predominant 11b-HSD1 oxo-reductase activity from both the intact ciliary body tissue (nZ12, median 2$1 pmol/mg per h and range 1$25-2$8 pmol/mg per h; PZ0$006) and primary cultures of corneal epithelial cells (nZ12, median 3$0 pmol/mg per h and range 1$0-7$4 pmol/mg per h, PZ0$008) compared with dehydrogenase activity (median 1$0 pmol/mg per h and range 0$5-2$0 pmol/mg per h; median 0$5 pmol/mg per h and range 0$25-1$9 pmol/mg per h respectively). These findings were supported by expression of 11b-HSD1 protein as visualised by Western blotting of ciliary body tissue and immunocytochemistry of corneal epithelial cells. Reduction of corneal epithelial cell proliferation was seen after primary cultures were co-incubated with cortisol and cortisone. 11b-HSD1 activity was not demonstrated in naïve conjunctival fibroblasts or corneal stromal keratocytes. Our results indicate that the distribution of 11b-HSD1 in the rabbit resembles that of the human eye and activates cortisone to cortisol in both corneal and uveal tissues. The NZWAR provides a suitable in vivo model for the further evaluation of 11b-HSD1 activity in the eye, especially its role in corneal epithelial and ciliary body physiology.

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“…The participation of mineralocorticoid hormones in ocular ion transport is in fact supported by a number of different observations such as: anticataractogenic influence of mineralocorticoids in experimental animals, opposite effects of cortisol and aldosterone in experimental cataract formation, elevated aldosterone in the lens of hypertensive patients, increased natremia and Na + in the aqueous humor of rabbits treated with aldosterone, development of glaucoma as a result of steroid hormone therapy, specific binding of aldosterone to the mineralocorticoid receptor (MCR) in rabbit lens epithelium [14], rabbit ciliary body [15] and isolated pigmentary epithelial cells [16]. Recently, we provided immunochemical evidence for the presence of the MCR [16,17] and ASSC [18] in a number of rodent ocular tissues in situ.…”

Section: Introductionmentioning

confidence: 92%

“…The notion that ocular sodium transport may be assured by the basolateral Na + -K + -ATPase [1][2][3][4] is not in keeping with the thermodynamic and other properties of the enzyme [5][6][7]. Second, circumstantial evidence suggests that steroid hormones play an important role in ocular sodium ion transport [14][15][16]. Since steroid signaling is the major determinant of ion-water homeostasis in many peripheral tissues and organs [8][9][10], it appeared logical to us that ocular sodium regulation may well follow a similar route.…”

Section: Discussionmentioning

confidence: 99%

Mineralocorticoid Hormone Signaling Regulates the ‘Epithelial Sodium Channel’ in Fibroblasts from Human Cornea

Mirshahi

Golestaneh

et al. 2000

Ophthalmic Res

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We investigated the regulation of sodium absorption by steroid hormones in embryologically diverse cells from the human eye. A cell extract from human corneal fibroblasts was positive for both the epithelial sodium channel (ENaC) and the mineralocorticoid receptor (MCR) as 82- to 85-kD and 102-kD bands, respectively, by the Western blot technique. In fluorescent, confocal and electron microscopy, the MCR was revealed as a nucleocytoplasmic protein, whereas the ENaC was almost exclusively membrane bound; both appeared aligned along actin filaments of corneal keratocytes, and both were widely colocalized in various cell types of human cornea in situ. Following reverse transcription and amplification of total RNA isolated from corneal fibroblasts, the ENaC and MCR genes in the PCR product were evident as predicted bands of 520 and 843 bp, respectively, whose sequence exhibited 100% identity with those from known human sources. The multiplication of corneal fibroblasts was influenced by both the MCR-specific antagonist RU 26752 and the natural hormone aldosterone, and these steroids also stimulated protein phosphorylation. In quantitative PCR, both the basal and aldosterone-induced levels of ENaC were diminished by the MCR-specific antagonist ZK 91587. Consequently, the ocular sodium channel appears to be regulated by steroid signalling in cells of diverse embryological origins, contrary to the existing notions where (a) this process would be limited exclusively to the epithelial cells and (b) ocular sodium transport would be regulated via the Na⁺-K⁺-ATPase in the basolateral membrane.

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Aldosterone: Its occurrence, metabolism and binding in the rabbit eye

Cited by 14 publications

References 11 publications

Mineralocorticoid Receptors in the Rabbit Iris-Ciliary Body

Mineralocorticoid Receptors in the Rabbit Iris-Ciliary Body

Characterisation of the prereceptor regulation of glucocorticoids in the anterior segment of the rabbit eye

Mineralocorticoid Hormone Signaling Regulates the ‘Epithelial Sodium Channel’ in Fibroblasts from Human Cornea

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