The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform
Shaul G. Massry - One of the best experts on this subject based on the ideXlab platform.
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Elevation of Cytosolic Calcium of rat cardiac myocytes in phosphate depletion
Kidney international, 1996Co-Authors: Yi-bin Zhang, Miroslaw Smogorzewski, Hung-hsiang Liou, Shaul G. MassryAbstract:Elevation of Cytosolic Calcium of rat cardiac myocytes in phosphate depletion. Phosphate depletion is associated with a rise in Cytosolic Calcium ([Ca 2+ ]i) of cells and such a derangement is responsible in major part for organ dysfunction in phosphate depletion (PD). Cardiac function is impaired in PD, and it is possible that PD is also associated with rise in [Ca 2+ ]i of cardiac myocytes. The present study examined the effect of PD on [Ca 2+ ]i of cardiac myocytes and explored the mechanisms that may lead to the rise in their [Ca 2+ ]i. The [Ca 2+ ]i of cardiac myocytes began to rise and ATP content began to fall at the third week of PD. After six weeks of PD, the values of [Ca 2+ ]i were significantly higher ( P P max of Ca 2+ -ATPase and Na + ,K + -ATPase as well as the Na + -Ca 2+ exchange were significantly lower ( P 2+ ]i of cardiac myocytes of PD rats is due to a decrease in Calcium efflux out of them.
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Parathyroid hormone increases Cytosolic Calcium concentration in adult rat cardiac myocytes
American Journal of Physiology-Heart and Circulatory Physiology, 1993Co-Authors: Miroslaw Smogorzewski, Maysa A. Zayed, Yi-bin Zhang, J. Roe, Shaul G. MassryAbstract:The heart is a target organ for parathyroid hormone (PTH), and the action of this hormone on the myocardium may be mediated through the ability of PTH to increase Cytosolic Calcium ([Ca2+]i) in the...
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Elevated Basal Levels of Cytosolic Calcium of Thymocytes in Chronic Renal Failure
American journal of nephrology, 1993Co-Authors: Olivera Stojceva-taneva, Miroslaw Smogorzewski, George Z. Fadda, Shaul G. MassryAbstract:The basal levels of Cytosolic Calcium ([Ca2+]i) in rats and/or humans with chronic renal failure (CRF) are elevated in many cells including brain synaptosomes, pancreatic islets,
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Parathyroid hormone raises Cytosolic Calcium in pancreatic islets: Study on mechanisms
Kidney international, 1993Co-Authors: George Z. Fadda, Miroslaw Smogorzewski, Prassert Thanakitcharu, Shaul G. MassryAbstract:Parathyroid hormone raises Cytosolic Calcium in pancreatic islets: Study on mechanisms. The pancreatic islets of Langerhans are targets for PTH and the action of the hormone on the islet is most likely mediated through the ability of PTH to increase Cytosolic Calcium ([Ca 2+ ] i ) of the islet cells. Although direct evidence for such an effect has been clearly demonstrated, the mechanisms through which the hormone exerts such an action are not elucidated. The present study examined these questions using pancreatic islets isolated from normal rats. Both 1-34 and 1-84 PTH produced a dose dependent increase in [Ca 2+ ] i of the islets but the effect of the latter was significantly (P 2+ i ]. Dibutyryl cAMP, and phorbol ester 12-myristate 13 acetate increased [Ca 2+ ] i of pancreatic islets in a dose dependent manner and the effect was inhibited (P 2+ ] i of the islets. These data indicate that: (1) PTH increases [Ca 2+ ] i of pancreatic islets, (2) this action is partly receptor mediated and is produced by activation of L-type Calcium channels through stimulation of G protein(s), and (3) the rise in [Ca 2+ ] i is due to both stimulation of cAMP generation and activation of protein kinase C.
David J. Handelsman - One of the best experts on this subject based on the ideXlab platform.
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CYCLIC ADENOSINE 3',5'-MONOPHOSPHATE-INDEPENDENT REGULATION OF Cytosolic Calcium IN SERTOLI CELLS
Endocrinology, 1996Co-Authors: E. Gorczynska, Jenny Spaliviero, David J. HandelsmanAbstract:We have examined the cAMP-independent regulation of Cytosolic Calcium concentration in rat Sertoli cells using the effect of vasoactive hormones, known as testicular paracrine regulators operating via the non-cAMP pathway, on Cytosolic Calcium. Calcium concentrations were estimated with dual excitation fluorimetry, using freshly isolated, fura-2/AM-loaded cells. No increase in the cellular cAMP concentration was detected after stimulation with angiotensin II (AII), vasopressin, PGF2 alpha, or atrial natriuretic peptide. Whereas both AII and vasopressin evoked a rise in Cytosolic Calcium from a basal level of 81.4 +/- 4 to 142.5 +/- 18 and 154.4 +/- 11 nM, respectively, PGF2 alpha had only a minimal effect (98 +/- 5 nM), and atrial natriuretic peptide no effect (86.6 +/- 9 nM). The effect of AII on Calcium was blocked by the the selective AT2, but not by the AT1, receptor antagonist, indicating the selective presence on Sertoli cells of AT2 AII receptor. Similarly, the vasopressin-induced Calcium response ...
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Androgens rapidly increase the Cytosolic Calcium concentration in Sertoli cells.
Endocrinology, 1995Co-Authors: E. Gorczynska, David J. HandelsmanAbstract:We demonstrate that androgens rapidly and specifically increase intracellular Calcium in Sertoli cells, investigate the mechanism, and suggest the unifying hypothesis that Calcium might be a common intracellular molecular effector to explain the known synergism between FSH and testosterone (T) action on Sertoli cells in support of spermatogenesis. In freshly isolated Sertoli cells, T and its 5 alpha-reduced metabolite dihydrotestosterone increased intracellular Calcium from 83 +/- 4 to 147 +/- 8 and 167 +/- 29 nM, respectively, whereas estradiol had minor (117 +/- 9 nM) and progesterone no (80 +/- 6 nM) effect. The effect of T was rapid (20-40 sec) and inhibited by 1) preincubation with either a pure nonsteroidal antiandrogen (hydroxyflutamide) or a 5 alpha-reductase inhibitor (finasteride) or 2) removal of extracellular Calcium (47 +/- 4 nM) or pharmacological blockade of voltage-activated (62 +/- 5 nM) or voltage-independent (55 +/- 14 nM) membrane Calcium channels. These findings suggest that the T-induced rise in Sertoli cell Cytosolic Calcium involves sequential 5 alpha-reduction, binding to a classical androgen receptor, and activation of transmembrane influx of extracellular Calcium. Immobilization of T by conjugation to a large carrier molecule (BSA) to prevent steroid entry into Sertoli cells also resulted in a rapid increase in Cytosolic Calcium to a similar magnitude as unconjugated T, consistent with a plasma membrane site of action. This finding together with the rapid Cytosolic Calcium rise caused by T argues for the possible existence of a short term, nongenomic effects in hormonal regulation of Sertoli cell function in addition to the well known, slower genomic response.
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Requirement for transmembrane sodium flux in maintenance of Cytosolic Calcium levels in rat Sertoli cells
American Journal of Physiology-Endocrinology and Metabolism, 1993Co-Authors: E. Gorczynska, David J. HandelsmanAbstract:The prompt rise in Cytosolic Calcium induced by follicle-stimulating hormone (FSH) in rat Sertoli cells suggests a role for Calcium in FSH signal transduction. To evaluate the requirement for sodium in transmembrane Calcium fluxes in Sertoli cells, we measured intracellular Calcium concentration under sodium-free conditions and during stimulation by monensin and veratridine, used to elevate Cytosolic sodium. Cytosolic Calcium levels were measured by dual-wavelength spectrofluorimetry using freshly isolated cells loaded with fura-2 acetoxymethyl ester. Whereas, removal of extracellular sodium lowered Cytosolic Calcium in unstimulated cells from 89 +/- 4 to 75 +/- 8 nM, treatment with monensin and veratridine increased Cytosolic Calcium to 142 +/- 19 and 126 +/- 13 nM, respectively. Without extracellular Calcium, monensin still produced 47% of the rise in Cytosolic Calcium observed in the presence of extracellular Calcium, indicating approximately equal contributions of Calcium from intracellular and extracellular sources. Blockade of voltage-sensitive or/and voltage-insensitive Calcium channels by verapamil and ruthenium red was unable to completely prevent the monensin-induced elevation of Cytosolic Calcium. In addition tetrodotoxin failed to block the FSH-induced rise in Cytosolic Calcium. These observations, together with the considerable reduction in monensin-induced rise in Cytosolic Calcium under extracellular sodium-free condition, support the hypothesis that sodium-Calcium exchange rather than the specific Calcium or sodium channels regulate basal and monensin-induced transmembrane sodium and Calcium fluxes in Sertoli cells.
Miroslaw Smogorzewski - One of the best experts on this subject based on the ideXlab platform.
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Elevation of Cytosolic Calcium of rat cardiac myocytes in phosphate depletion
Kidney international, 1996Co-Authors: Yi-bin Zhang, Miroslaw Smogorzewski, Hung-hsiang Liou, Shaul G. MassryAbstract:Elevation of Cytosolic Calcium of rat cardiac myocytes in phosphate depletion. Phosphate depletion is associated with a rise in Cytosolic Calcium ([Ca 2+ ]i) of cells and such a derangement is responsible in major part for organ dysfunction in phosphate depletion (PD). Cardiac function is impaired in PD, and it is possible that PD is also associated with rise in [Ca 2+ ]i of cardiac myocytes. The present study examined the effect of PD on [Ca 2+ ]i of cardiac myocytes and explored the mechanisms that may lead to the rise in their [Ca 2+ ]i. The [Ca 2+ ]i of cardiac myocytes began to rise and ATP content began to fall at the third week of PD. After six weeks of PD, the values of [Ca 2+ ]i were significantly higher ( P P max of Ca 2+ -ATPase and Na + ,K + -ATPase as well as the Na + -Ca 2+ exchange were significantly lower ( P 2+ ]i of cardiac myocytes of PD rats is due to a decrease in Calcium efflux out of them.
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Parathyroid hormone increases Cytosolic Calcium concentration in adult rat cardiac myocytes
American Journal of Physiology-Heart and Circulatory Physiology, 1993Co-Authors: Miroslaw Smogorzewski, Maysa A. Zayed, Yi-bin Zhang, J. Roe, Shaul G. MassryAbstract:The heart is a target organ for parathyroid hormone (PTH), and the action of this hormone on the myocardium may be mediated through the ability of PTH to increase Cytosolic Calcium ([Ca2+]i) in the...
-
Elevated Basal Levels of Cytosolic Calcium of Thymocytes in Chronic Renal Failure
American journal of nephrology, 1993Co-Authors: Olivera Stojceva-taneva, Miroslaw Smogorzewski, George Z. Fadda, Shaul G. MassryAbstract:The basal levels of Cytosolic Calcium ([Ca2+]i) in rats and/or humans with chronic renal failure (CRF) are elevated in many cells including brain synaptosomes, pancreatic islets,
-
Parathyroid hormone raises Cytosolic Calcium in pancreatic islets: Study on mechanisms
Kidney international, 1993Co-Authors: George Z. Fadda, Miroslaw Smogorzewski, Prassert Thanakitcharu, Shaul G. MassryAbstract:Parathyroid hormone raises Cytosolic Calcium in pancreatic islets: Study on mechanisms. The pancreatic islets of Langerhans are targets for PTH and the action of the hormone on the islet is most likely mediated through the ability of PTH to increase Cytosolic Calcium ([Ca 2+ ] i ) of the islet cells. Although direct evidence for such an effect has been clearly demonstrated, the mechanisms through which the hormone exerts such an action are not elucidated. The present study examined these questions using pancreatic islets isolated from normal rats. Both 1-34 and 1-84 PTH produced a dose dependent increase in [Ca 2+ ] i of the islets but the effect of the latter was significantly (P 2+ i ]. Dibutyryl cAMP, and phorbol ester 12-myristate 13 acetate increased [Ca 2+ ] i of pancreatic islets in a dose dependent manner and the effect was inhibited (P 2+ ] i of the islets. These data indicate that: (1) PTH increases [Ca 2+ ] i of pancreatic islets, (2) this action is partly receptor mediated and is produced by activation of L-type Calcium channels through stimulation of G protein(s), and (3) the rise in [Ca 2+ ] i is due to both stimulation of cAMP generation and activation of protein kinase C.
E. Gorczynska - One of the best experts on this subject based on the ideXlab platform.
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CYCLIC ADENOSINE 3',5'-MONOPHOSPHATE-INDEPENDENT REGULATION OF Cytosolic Calcium IN SERTOLI CELLS
Endocrinology, 1996Co-Authors: E. Gorczynska, Jenny Spaliviero, David J. HandelsmanAbstract:We have examined the cAMP-independent regulation of Cytosolic Calcium concentration in rat Sertoli cells using the effect of vasoactive hormones, known as testicular paracrine regulators operating via the non-cAMP pathway, on Cytosolic Calcium. Calcium concentrations were estimated with dual excitation fluorimetry, using freshly isolated, fura-2/AM-loaded cells. No increase in the cellular cAMP concentration was detected after stimulation with angiotensin II (AII), vasopressin, PGF2 alpha, or atrial natriuretic peptide. Whereas both AII and vasopressin evoked a rise in Cytosolic Calcium from a basal level of 81.4 +/- 4 to 142.5 +/- 18 and 154.4 +/- 11 nM, respectively, PGF2 alpha had only a minimal effect (98 +/- 5 nM), and atrial natriuretic peptide no effect (86.6 +/- 9 nM). The effect of AII on Calcium was blocked by the the selective AT2, but not by the AT1, receptor antagonist, indicating the selective presence on Sertoli cells of AT2 AII receptor. Similarly, the vasopressin-induced Calcium response ...
-
Androgens rapidly increase the Cytosolic Calcium concentration in Sertoli cells.
Endocrinology, 1995Co-Authors: E. Gorczynska, David J. HandelsmanAbstract:We demonstrate that androgens rapidly and specifically increase intracellular Calcium in Sertoli cells, investigate the mechanism, and suggest the unifying hypothesis that Calcium might be a common intracellular molecular effector to explain the known synergism between FSH and testosterone (T) action on Sertoli cells in support of spermatogenesis. In freshly isolated Sertoli cells, T and its 5 alpha-reduced metabolite dihydrotestosterone increased intracellular Calcium from 83 +/- 4 to 147 +/- 8 and 167 +/- 29 nM, respectively, whereas estradiol had minor (117 +/- 9 nM) and progesterone no (80 +/- 6 nM) effect. The effect of T was rapid (20-40 sec) and inhibited by 1) preincubation with either a pure nonsteroidal antiandrogen (hydroxyflutamide) or a 5 alpha-reductase inhibitor (finasteride) or 2) removal of extracellular Calcium (47 +/- 4 nM) or pharmacological blockade of voltage-activated (62 +/- 5 nM) or voltage-independent (55 +/- 14 nM) membrane Calcium channels. These findings suggest that the T-induced rise in Sertoli cell Cytosolic Calcium involves sequential 5 alpha-reduction, binding to a classical androgen receptor, and activation of transmembrane influx of extracellular Calcium. Immobilization of T by conjugation to a large carrier molecule (BSA) to prevent steroid entry into Sertoli cells also resulted in a rapid increase in Cytosolic Calcium to a similar magnitude as unconjugated T, consistent with a plasma membrane site of action. This finding together with the rapid Cytosolic Calcium rise caused by T argues for the possible existence of a short term, nongenomic effects in hormonal regulation of Sertoli cell function in addition to the well known, slower genomic response.
-
Requirement for transmembrane sodium flux in maintenance of Cytosolic Calcium levels in rat Sertoli cells
American Journal of Physiology-Endocrinology and Metabolism, 1993Co-Authors: E. Gorczynska, David J. HandelsmanAbstract:The prompt rise in Cytosolic Calcium induced by follicle-stimulating hormone (FSH) in rat Sertoli cells suggests a role for Calcium in FSH signal transduction. To evaluate the requirement for sodium in transmembrane Calcium fluxes in Sertoli cells, we measured intracellular Calcium concentration under sodium-free conditions and during stimulation by monensin and veratridine, used to elevate Cytosolic sodium. Cytosolic Calcium levels were measured by dual-wavelength spectrofluorimetry using freshly isolated cells loaded with fura-2 acetoxymethyl ester. Whereas, removal of extracellular sodium lowered Cytosolic Calcium in unstimulated cells from 89 +/- 4 to 75 +/- 8 nM, treatment with monensin and veratridine increased Cytosolic Calcium to 142 +/- 19 and 126 +/- 13 nM, respectively. Without extracellular Calcium, monensin still produced 47% of the rise in Cytosolic Calcium observed in the presence of extracellular Calcium, indicating approximately equal contributions of Calcium from intracellular and extracellular sources. Blockade of voltage-sensitive or/and voltage-insensitive Calcium channels by verapamil and ruthenium red was unable to completely prevent the monensin-induced elevation of Cytosolic Calcium. In addition tetrodotoxin failed to block the FSH-induced rise in Cytosolic Calcium. These observations, together with the considerable reduction in monensin-induced rise in Cytosolic Calcium under extracellular sodium-free condition, support the hypothesis that sodium-Calcium exchange rather than the specific Calcium or sodium channels regulate basal and monensin-induced transmembrane sodium and Calcium fluxes in Sertoli cells.
Yi-bin Zhang - One of the best experts on this subject based on the ideXlab platform.
-
Elevation of Cytosolic Calcium of rat cardiac myocytes in phosphate depletion
Kidney international, 1996Co-Authors: Yi-bin Zhang, Miroslaw Smogorzewski, Hung-hsiang Liou, Shaul G. MassryAbstract:Elevation of Cytosolic Calcium of rat cardiac myocytes in phosphate depletion. Phosphate depletion is associated with a rise in Cytosolic Calcium ([Ca 2+ ]i) of cells and such a derangement is responsible in major part for organ dysfunction in phosphate depletion (PD). Cardiac function is impaired in PD, and it is possible that PD is also associated with rise in [Ca 2+ ]i of cardiac myocytes. The present study examined the effect of PD on [Ca 2+ ]i of cardiac myocytes and explored the mechanisms that may lead to the rise in their [Ca 2+ ]i. The [Ca 2+ ]i of cardiac myocytes began to rise and ATP content began to fall at the third week of PD. After six weeks of PD, the values of [Ca 2+ ]i were significantly higher ( P P max of Ca 2+ -ATPase and Na + ,K + -ATPase as well as the Na + -Ca 2+ exchange were significantly lower ( P 2+ ]i of cardiac myocytes of PD rats is due to a decrease in Calcium efflux out of them.
-
Parathyroid hormone increases Cytosolic Calcium concentration in adult rat cardiac myocytes
American Journal of Physiology-Heart and Circulatory Physiology, 1993Co-Authors: Miroslaw Smogorzewski, Maysa A. Zayed, Yi-bin Zhang, J. Roe, Shaul G. MassryAbstract:The heart is a target organ for parathyroid hormone (PTH), and the action of this hormone on the myocardium may be mediated through the ability of PTH to increase Cytosolic Calcium ([Ca2+]i) in the...
