Blocking Urinary Electrolyte Effects of Desoxycorticosterone with Progesterone in Rats.

Kagawa, C. M.

doi:10.3181/00379727-99-24471

Cited by 41 publications

(14 citation statements)

References 1 publication

(3 reference statements)

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“…Prog activation of the MR is unexpected because Prog is an antagonist for wild-type human MR (Kagawa 1958, Wambach & Higgins 1978, Funder & Adam 1981, Rupprecht et al 1993b, Geller et al 2000, Rafestin-Oblin et al 2003, Sugimoto et al 2016. The mineralocorticoid activity of Prog for Leu-810 MR explained high blood pressure in pregnant woman with this mutant MR.…”

Section: Evolution Of the Contact Between Ser810 (Helix 5) And Ala773mentioning

confidence: 99%

“…In this regard, allosteric interactions between the A/B domain and the ligand-binding domain also are important in differences among corticosteroids in transcriptional activation of the GR (Pearce & Yamamoto 1993, Rupprecht et al 1993a, Oka et al 2015. Interestingly, Prog is an antagonist for human MR (Kagawa 1958, Wambach & Higgins 1978, Funder & Adam 1981, Rupprecht et al 1993b, Geller et al 2000, Sugimoto et al 2016.…”

Section: Introductionmentioning

confidence: 99%

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30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Evolution of the mineralocorticoid receptor: sequence, structure and function

Baker

Katsu

2017

Journal of Endocrinology

124

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The mineralocorticoid receptor (MR) is descended from a corticoid receptor (CR), which has descendants in lamprey and hagfish, cyclostomes (jawless fish), a taxon that evolved at the base of the vertebrate line. A distinct MR and GR first appear in cartilaginous fishes (Chondrichthyes), such as sharks, skates, rays and chimeras. Skate MR has a strong response to corticosteroids that are mineralocorticoids and glucocorticoids in humans. The half-maximal responses (EC50s) for skate MR for the mineralocorticoids aldosterone and 11-deoxycorticosterone are 0.07 nM and 0.03 nM, respectively. EC50s for the glucocorticoids cortisol and corticosterone are 1 nM and 0.09 nM, respectively. The physiological mineralocorticoid in ray-finned fish, which do not synthesize aldosterone, is not fully understood because several 3-ketosteroids, including cortisol, 11-deoxycortisol, corticosterone, 11-deoxycorticosterone and progesterone are transcriptional activators of fish MR. Further divergence of the MR and GR in terrestrial vertebrates, which synthesize aldosterone, led to emergence of aldosterone as a selective ligand for the MR. Here, we combine sequence analysis of the CR and vertebrate MRs and GRs, analysis of crystal structures of human MR and GR and data on transcriptional activation by 3-ketosteroids of wild-type and mutant MRs and GRs to investigate the evolution of selectivity for 3-ketosteroids by the MR in terrestrial vertebrates and ray-finned fish, as well as the basis for binding of some glucocorticoids by human MR and other vertebrate MRs.

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Section: Evolution Of the Contact Between Ser810 (Helix 5) And Ala773mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Evolution of the mineralocorticoid receptor: sequence, structure and function

Baker

Katsu

2017

Journal of Endocrinology

124

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“…Progesterone increases urinary sodium excretion in the presence of an endogen¬ ous or exogenous mineralocortocoid active hormone in experimental animal and man (Landau et al 1955;Kagawa 1958;Sundsfjord 1971;Wambach 8c Higgins 1978). This natriuretic effect or progesterone correlates with its ability to displace [:iH] aldosterone from binding at rat renal mineralocorticoid recep¬ tors (Wambach 8c Higgins 1978).…”

mentioning

confidence: 97%

Interaction of Synthetic Progestagens With Renal Mineralocorticoid Receptors

Wambach¹,

Higgins²,

Kern³

et al. 1979

Acta Endocrinologica

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Progesterone increases urinary sodium excretion at least in part by competition for renal mineralocorticoid receptors. In contrast, synthetic progestagens do not increase sodium excretion or even cause a slight sodium retention. We therefore compared the ability of progesterone and 12 progesterone like compounds to displace [3H] aldosterone from binding at cytoplasmic mineralocorticoid receptors in rat kidney. All synthetic progesteronelike steroids were less active than progesterone in competing with [3H]aldosterone for the receptor binding: progesterone 100 %, 1 1 \ g = b \ \ x = r e q -\ Trivial and systematic names Progesterone: 11 ß OH-progesterone: ¡7 OH-progesterone: ¡6 methyl-progesterone: Medrogestone: Dydrogesterone: Medroxyprogesterone acetate: Chlormadinone acetate: Ethisterone: Norethynodrel: Ethynodiol-diacetate: Norethisterone: Norethindrone-acetate :Spironolactone: of steroids 4-pregnene-3,20-dione ¡ 1 /?-hydroxy-4-pregnene-3,20-dione ¡ 7 a-hydroxy-4-pregnene-3,20-dione ¡6 a-metyl-4-pregnene-3,20-dione 6 a-methyl-¡7 a-hydroxy-4-pregnene-3,20-dione 9 ß, ¡0 a-pregna-4,6-diene-3,20-dione 6 -methyl-17 a-hydroxy-4-pregnene-3,20-dione acetate 6-chloro-17 a-hydroxy4,6-pregnadiene-3,20-dione acetate ¡7 a-ethynyl-¡7 /7-hydroxy-4-oestren-3-one 17 a-ethynyl-i7 /)-hydroxy-5(10)oestren-3-one ¡7 a-ethynyl-3 ß-\7 /S-dihydroxy-4-oestren-diacetate 17 a-ethynyl-17 /?-hydroxy-4-oestren-3-one ¡7 a-ethynyl-17 /7hydroxy-4-oestren-3-one-acetate potassium 3-(3-oxo-i7 /?-hydroxy-4,6-androstadiene-¡7-a-yl) propionate

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“…of deoxycorticosterone acetate, but in higher dosage progesterone had a sodium-retaining effect. 177 An antagonistic effect of progesterone on the sodium-retaining action of aldosterone, but not on its potassium-losing action, in the adrenalectomized rat has also been noted. 353 Progesterone likewise antagonizes the stimulatory effect of aldosterone on sodium transpOlt across the isolated toad bladder.SG A synthetic derivative 1,4-pregnadiene,3,15,20-trione, also has blocking activity.…”

mentioning

confidence: 99%