| 1. |
- Ivanova, L N, et al.
(författare)
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[Vasopressin : the ontogeny of antidiuretic action at the cellular level].
- 1989
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Ingår i: Fiziologicheskiĭ zhurnal SSSR imeni I. M. Sechenova. - 0015-329X. ; 75:7, s. 970-9
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Tidskriftsartikel (refereegranskat)abstract
- The data on the development of molecular mechanism of the antidiuretic effect of vasopressin and the molecular structure of the AVP receptor, cytosolic cAMP-dependent protein-kinases and renal response to AVP, are discussed. The experiments were performed in normal rats and mice, nephrogenic diabetes insipidus mutants and rats treated with cortisol in early postnatal period. The development of the kidney sensitivity to AVP seems to be closely connected with the development of the molecular structure of the AVP receptor, age-related increase of the AVP-activated adenylate cyclase, and the maturation of cAMP-dependent protein kinases.
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| 2. |
- Solenov, E I, et al.
(författare)
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[Changes in the receptor link during the development of renal sensitivity to aldosterone and antidiuretic hormone].
- 1986
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Ingår i: Fiziologicheskiĭ zhurnal SSSR imeni I. M. Sechenova. - 0015-329X. ; 72:12, s. 1673-9
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Tidskriftsartikel (refereegranskat)abstract
- The aldosterone, cAMP and ADH receptors were studied in kidneys of 10-14- and 60-day old rats. Concentrations of aldosterone and cAMP receptors were reduced, while ADH binding was increased during the period of maturation of kidney functions. The investigation of the affinity and molecular weights of cAMP and ADH receptors suggests their complex nature and altering of their individual properties during ontogenesis. Aldosterone and cAMP with their receptors seem to participate in the regulation of gene activity in ontogenesis and ADH seems to participate in the formation of its own receptors.
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| 3. |
- Zelenina, M N, et al.
(författare)
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[Activity of cAMP-dependent protein kinases and cAMP-binding proteins from rat renal cytosol upon dehydration].
- 1985
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Ingår i: Biokhimii͡a (Moscow, Russia). - 0320-9725. ; 50:3, s. 439-42
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Tidskriftsartikel (refereegranskat)abstract
- The activity of cAMP-dependent protein kinases, cAMP binding and the spectrum of cAMP-binding proteins in renal papillary cytosol of intact rats and of rats kept on a water-deprived diet for 24 hours were investigated. It was found that the stimulation of protein kinases by 10(-6) M cAMP in the experimental group was significantly higher than in the control one. On DEAE-cellulose chromatography, the position of peaks of the specific cAMP binding corresponded to those of the regulatory cAMP-dependent protein kinases type I and II. Under these conditions, more than 80% of the binding activity in intact animals was localized in peak II, whereas in rats kept on a water-deprived diet over 60% of the binding activity was localized in peak I. The total binding activity of cytosol in experimental animals remained unchanged is compared to intact rats. It is suggested that in renal papilla dehydration is accompanied by the induction of synthesis of regulatory subunits of cAMP-dependent protein kinase type I.
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| 4. |
- Zelenina, M N, et al.
(författare)
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[Changes in cAMP reception in the cytosol of the developing rat kidney].
- 1986
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Ingår i: Biokhimii͡a (Moscow, Russia). - 0320-9725. ; 51:1, s. 77-9
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Tidskriftsartikel (refereegranskat)abstract
- The age-dependent changes in the cAMP-binding activity of renal papillary cytosol were studied in intact rats and in animals with experimental delay in development of the concentrating renal function induced by hydrocortisone injection in early postnatal period. The age dynamics of specific cAMP binding in the experimental group differ significantly from that in intact and control (sham injected) animals. It is suggested that the developmental changes in experimental animal kidneys are due to disturbances in hormonal regulation of renal tissue differentiation caused by the changes in intracellular receptors of cAMP. Another possible reason for the observed delay of development of the renal function is the weakening of the stimulating effect of endogenous cAMP on the genome function due to cAMP receptor deficiency in the cell.
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