Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 399 (1983), S. 93-101 
    ISSN: 1432-2013
    Keywords: Aldosterone ; 9-Alpha fluorocortisol ; Deoxycorticosterone ; Dexamethasone ; Spironolactone ; Glomerular filtration rate ; Urinary Na/K ratio ; Sprague-Dawley rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The acute effects of mineralo- and glucocorticoids on urinary electrolyte excretion were studied in the conscious, acutely potassium deprived, adrenalectomized rat. Sodium, potassium, and creatinine were measured in the urine excreted from 2.5 to 5.5 h after injection of one or more of the following steroids: aldosterone (Aldo), 9-alpha fluorocortisol (FC), deoxycorticosterone (DOC), dexamethasone (Dex), and spironolactone (Spiro). The hierarchy (a) for increasing creatinine excretion was Dex〉FC〉Aldo〉DOC〉Spiro 〉none, a hierarchy consistent with glucocorticoid potency; and (b) for producing anti-natriuresis was Aldo〉DOC≥FC ≥none=Spiro〉Dex, a hierarchy consistent with mineralocorticoid potency. In contrast, the kaliuresis produced by mineralo- and glucocorticoids appears different. A “mineralocorticoid” kaliuresis is 1) elicited by anti-natriuretic doses of Aldo and FC, 2) approximately twice control UKV, 3) unrelated to changes in glomerular filtration rate (GFR), and 4) inhibited by Spiro. A “glucocorticoid” kaliuresis is 1) elicited by Dex and high doses of Aldo and FC, 2) about seven to twenty-fold greater than control UKV, 3) possibly dependent, in part, on changes in GFR, and, 4) not inhibited by Spiro. DOC was not kaliuretic at anti-natriuretic doses. The urinary Na/K ratio was an unreliable index of mineralocorticoid action.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 40 (1978), S. 199-211 
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Urinary acidification by the urinary bladder of the toad (Bufo marinus) was stimulated, relative to control, by thein vitro addition of aldosterone (10−7 m), actinomycin D (20 μg/ml), puromycin (80 μg/ml) or cycloheximide (5 μg/ml). The action of the inhibitors of RNA or protein synthesis was not additive with that of aldosterone. This is opposite to the situation with Na+ transport, where the stimulation by aldosterone is abolished by the same concentrations of these inhibitors. That all agents enhanced urinary acidification was verified by: (i) measurement of RSCC (reverse short-circuit current) in the absence of Na+ transport, (ii) inhibition of RSCC by acetazolamide, an inhibitor of carbonic anhydrase, and (iii) direct measurement of the pH change of the mucosal (urinary) fluid. As in the case of Na+ transport, spirolactone inhibited the action of aldosterone. Although not a unique model, the apparent paradoxical mimicry of aldosterone's stimulation of urinary acidification may be explained by a model which includes action of aldosterone and the inhibitors via their known effects on RNA and protein synthesis.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Supramolecular Structure 9 (1978), S. 421-426 
    ISSN: 0091-7419
    Keywords: aldosterone ; dexamethasone ; dihydrotestosterone ; estrogen ; progesterone ; steroid hormone receptor ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Binding of steroid hormones is inhibited by protease inhibitors and substrates. The protease inhibitors phenylmethyl sulphonylfluoride, tosyl-lysine chloromethyl ketone, and tosylamide-phenylethyl-chloromethyl ketone and the protease substrates tosyl arginine methyl ester and tryptophan methyl ester eliminate specific binding of aldosterone, dexamethasone, dihydrotestosterone, estrogen, and progesterone to their respective receptors. These protease inhibitors and substrates also inhibit binding of progesterone to the 20,000 molecular weight mero-receptor formed from the progesterone receptor in chick oviduct. The binding of estradiol to rat alpha-fetoprotein is inhibited by the protease inhibitors and substrates but not by tryptophan or tryptophan amide, indicating the importance of an ester structure in the inhibition of steroid binding. Our results suggest that all steroid hormone receptors have a site with both common structural features and a role in the regulation of steroid hormone binding.
    Additional Material: 5 Tab.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...