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Penelope A. Longhurst - One of the best experts on this subject based on the ideXlab platform.

  • comparison of urinary bladder function in rats with hereditary Diabetes insipidus streptozotocin induced Diabetes Mellitus and nondiabetic osmotic diuresis
    The Journal of Urology, 1994
    Co-Authors: Berit Eika, Penelope A. Longhurst, Robert M. Levin
    Abstract:

    Abstract In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary Diabetes insipidus (di/di), 2) Sprague-Dawley rats with Streptozotocin-Induced Diabetes Mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental Diabetes Mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cystometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.

  • comparison of urinary bladder function in rats with hereditary Diabetes insipidus streptozotocin induced Diabetes Mellitus and nondiabetic osmotic diuresis
    The Journal of Urology, 1994
    Co-Authors: Berit Eika, Penelope A. Longhurst, Robert M. Levin
    Abstract:

    In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary Diabetes insipidus (di/di), 2) Sprague-Dawley rats with Streptozotocin-Induced Diabetes Mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in the STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental Diabetes Mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cytometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.

  • the influence of streptozotocin induced Diabetes Mellitus on the sensitivity of rat urinary bladder body and base strips to changes in extracellular calcium
    General Pharmacology-the Vascular System, 1992
    Co-Authors: Penelope A. Longhurst, Robert E. Leggett, Thomas P Brotcke, Robert M. Levin
    Abstract:

    Abstract 1. 1. The influence of calcium on contractile responses of bladders from control and 2 month streptozotocin-diabetic rats was investigated. 2. 2. Removal of calcium from the bathing medium caused rapid decreases in the contractile responses of bladder body and base strips to carbachol. The responses of strips from control rats were reduced more by calcium removal than were strips from diabetics. 3. 3. Replacement of calcium caused dose-dependent increases in contraction to carbachol. The responses of bladder body strips from diabetic rats to carbachol were significantly greater at all calcium concentrations than were those of controls. There were no differences in the responsiveness of bladder base strips to carbachol. 4. 4. In contrast, bladder body strips from diabetic rats were more sensitive to calcium than were strips from controls, with an IC 50 value for calcium of 0.38 mM vs 0.72 mM for controls. 5. 5. At the calcium concentration of Krebs buffer (2.5 mM), contractile responses were near maximal, and there were no differences in sensitivity. 6. 6. The calcium antagonist nifedipine caused dose-dependent decreases in the contractile responses of bladder base and body strips to nerve stimulation. The responses to nerve stimulation were more sensitive to nifedipine than were those to carbachol. There were no differences between controls and diabetics in the sensitivity of bladder strips to nifedipine. 7. 7. The findings suggest that although increases in sensitivity to calcium are observed in bladder body strips from streptozotocin-diabetic rats, they are unlikely to be responsible for the increases in maximal contractile response to nerve stimulation and contractile agents.

Robert M. Levin - One of the best experts on this subject based on the ideXlab platform.

  • comparison of urinary bladder function in rats with hereditary Diabetes insipidus streptozotocin induced Diabetes Mellitus and nondiabetic osmotic diuresis
    The Journal of Urology, 1994
    Co-Authors: Berit Eika, Penelope A. Longhurst, Robert M. Levin
    Abstract:

    Abstract In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary Diabetes insipidus (di/di), 2) Sprague-Dawley rats with Streptozotocin-Induced Diabetes Mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental Diabetes Mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cystometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.

  • comparison of urinary bladder function in rats with hereditary Diabetes insipidus streptozotocin induced Diabetes Mellitus and nondiabetic osmotic diuresis
    The Journal of Urology, 1994
    Co-Authors: Berit Eika, Penelope A. Longhurst, Robert M. Levin
    Abstract:

    In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary Diabetes insipidus (di/di), 2) Sprague-Dawley rats with Streptozotocin-Induced Diabetes Mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in the STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental Diabetes Mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cytometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.

  • the influence of streptozotocin induced Diabetes Mellitus on the sensitivity of rat urinary bladder body and base strips to changes in extracellular calcium
    General Pharmacology-the Vascular System, 1992
    Co-Authors: Penelope A. Longhurst, Robert E. Leggett, Thomas P Brotcke, Robert M. Levin
    Abstract:

    Abstract 1. 1. The influence of calcium on contractile responses of bladders from control and 2 month streptozotocin-diabetic rats was investigated. 2. 2. Removal of calcium from the bathing medium caused rapid decreases in the contractile responses of bladder body and base strips to carbachol. The responses of strips from control rats were reduced more by calcium removal than were strips from diabetics. 3. 3. Replacement of calcium caused dose-dependent increases in contraction to carbachol. The responses of bladder body strips from diabetic rats to carbachol were significantly greater at all calcium concentrations than were those of controls. There were no differences in the responsiveness of bladder base strips to carbachol. 4. 4. In contrast, bladder body strips from diabetic rats were more sensitive to calcium than were strips from controls, with an IC 50 value for calcium of 0.38 mM vs 0.72 mM for controls. 5. 5. At the calcium concentration of Krebs buffer (2.5 mM), contractile responses were near maximal, and there were no differences in sensitivity. 6. 6. The calcium antagonist nifedipine caused dose-dependent decreases in the contractile responses of bladder base and body strips to nerve stimulation. The responses to nerve stimulation were more sensitive to nifedipine than were those to carbachol. There were no differences between controls and diabetics in the sensitivity of bladder strips to nifedipine. 7. 7. The findings suggest that although increases in sensitivity to calcium are observed in bladder body strips from streptozotocin-diabetic rats, they are unlikely to be responsible for the increases in maximal contractile response to nerve stimulation and contractile agents.

Berit Eika - One of the best experts on this subject based on the ideXlab platform.

  • comparison of urinary bladder function in rats with hereditary Diabetes insipidus streptozotocin induced Diabetes Mellitus and nondiabetic osmotic diuresis
    The Journal of Urology, 1994
    Co-Authors: Berit Eika, Penelope A. Longhurst, Robert M. Levin
    Abstract:

    Abstract In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary Diabetes insipidus (di/di), 2) Sprague-Dawley rats with Streptozotocin-Induced Diabetes Mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental Diabetes Mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cystometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.

  • comparison of urinary bladder function in rats with hereditary Diabetes insipidus streptozotocin induced Diabetes Mellitus and nondiabetic osmotic diuresis
    The Journal of Urology, 1994
    Co-Authors: Berit Eika, Penelope A. Longhurst, Robert M. Levin
    Abstract:

    In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary Diabetes insipidus (di/di), 2) Sprague-Dawley rats with Streptozotocin-Induced Diabetes Mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in the STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental Diabetes Mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cytometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.

Alfred L Goldberg - One of the best experts on this subject based on the ideXlab platform.

  • multiple types of skeletal muscle atrophy involve a common program of changes in gene expression
    The FASEB Journal, 2004
    Co-Authors: Stewart H Lecker, Thomas R Jagoe, Alexander Gilbert, Marcelo Gomes, Vickie E Baracos, James L Bailey, Russ S Price, William E Mitch, Alfred L Goldberg
    Abstract:

    Skeletal muscle atrophy is a debilitating response to starvation and many systemic diseases including Diabetes, cancer, and renal failure. We had proposed that a common set of transcriptional adaptations underlie the loss of muscle mass in these different states. To test this hypothesis, we used cDNA microarrays to compare the changes in content of specific mRNAs in muscles atrophying from different causes. We compared muscles from fasted mice, from rats with cancer cachexia, Streptozotocin-Induced Diabetes Mellitus, uremia induced by subtotal nephrectomy, and from pair-fed control rats. Although the content of >90% of mRNAs did not change, including those for the myofibrillar apparatus, we found a common set of genes (termed atrogins) that were induced or suppressed in muscles in these four catabolic states. Among the strongly induced genes were many involved in protein degradation, including polyubiquitins, Ub fusion proteins, the Ub ligases atrogin-1/MAFbx and MuRF-1, multiple but not all subunits of t...

  • multiple types of skeletal muscle atrophy involve a common program of changes in gene expression
    The FASEB Journal, 2004
    Co-Authors: Stewart H Lecker, Thomas R Jagoe, Alexander Gilbert, Marcelo Gomes, Vickie E Baracos, James L Bailey, Russ S Price, William E Mitch, Alfred L Goldberg
    Abstract:

    Skeletal muscle atrophy is a debilitating response to starvation and many systemic diseases including Diabetes, cancer, and renal failure. We had proposed that a common set of transcriptional adaptations underlie the loss of muscle mass in these different states. To test this hypothesis, we used cDNA microarrays to compare the changes in content of specific mRNAs in muscles atrophying from different causes. We compared muscles from fasted mice, from rats with cancer cachexia, Streptozotocin-Induced Diabetes Mellitus, uremia induced by subtotal nephrectomy, and from pair-fed control rats. Although the content of >90% of mRNAs did not change, including those for the myofibrillar apparatus, we found a common set of genes (termed atrogins) that were induced or suppressed in muscles in these four catabolic states. Among the strongly induced genes were many involved in protein degradation, including polyubiquitins, Ub fusion proteins, the Ub ligases atrogin-1/MAFbx and MuRF-1, multiple but not all subunits of the 20S proteasome and its 19S regulator, and cathepsin L. Many genes required for ATP production and late steps in glycolysis were down-regulated, as were many transcripts for extracellular matrix proteins. Some genes not previously implicated in muscle atrophy were dramatically up-regulated (lipin, metallothionein, AMP deaminase, RNA helicase-related protein, TG interacting factor) and several growth-related mRNAs were down-regulated (P311, JUN, IGF-1-BP5). Thus, different types of muscle atrophy share a common transcriptional program that is activated in many systemic diseases.

Stewart H Lecker - One of the best experts on this subject based on the ideXlab platform.

  • multiple types of skeletal muscle atrophy involve a common program of changes in gene expression
    The FASEB Journal, 2004
    Co-Authors: Stewart H Lecker, Thomas R Jagoe, Alexander Gilbert, Marcelo Gomes, Vickie E Baracos, James L Bailey, Russ S Price, William E Mitch, Alfred L Goldberg
    Abstract:

    Skeletal muscle atrophy is a debilitating response to starvation and many systemic diseases including Diabetes, cancer, and renal failure. We had proposed that a common set of transcriptional adaptations underlie the loss of muscle mass in these different states. To test this hypothesis, we used cDNA microarrays to compare the changes in content of specific mRNAs in muscles atrophying from different causes. We compared muscles from fasted mice, from rats with cancer cachexia, Streptozotocin-Induced Diabetes Mellitus, uremia induced by subtotal nephrectomy, and from pair-fed control rats. Although the content of >90% of mRNAs did not change, including those for the myofibrillar apparatus, we found a common set of genes (termed atrogins) that were induced or suppressed in muscles in these four catabolic states. Among the strongly induced genes were many involved in protein degradation, including polyubiquitins, Ub fusion proteins, the Ub ligases atrogin-1/MAFbx and MuRF-1, multiple but not all subunits of t...

  • multiple types of skeletal muscle atrophy involve a common program of changes in gene expression
    The FASEB Journal, 2004
    Co-Authors: Stewart H Lecker, Thomas R Jagoe, Alexander Gilbert, Marcelo Gomes, Vickie E Baracos, James L Bailey, Russ S Price, William E Mitch, Alfred L Goldberg
    Abstract:

    Skeletal muscle atrophy is a debilitating response to starvation and many systemic diseases including Diabetes, cancer, and renal failure. We had proposed that a common set of transcriptional adaptations underlie the loss of muscle mass in these different states. To test this hypothesis, we used cDNA microarrays to compare the changes in content of specific mRNAs in muscles atrophying from different causes. We compared muscles from fasted mice, from rats with cancer cachexia, Streptozotocin-Induced Diabetes Mellitus, uremia induced by subtotal nephrectomy, and from pair-fed control rats. Although the content of >90% of mRNAs did not change, including those for the myofibrillar apparatus, we found a common set of genes (termed atrogins) that were induced or suppressed in muscles in these four catabolic states. Among the strongly induced genes were many involved in protein degradation, including polyubiquitins, Ub fusion proteins, the Ub ligases atrogin-1/MAFbx and MuRF-1, multiple but not all subunits of the 20S proteasome and its 19S regulator, and cathepsin L. Many genes required for ATP production and late steps in glycolysis were down-regulated, as were many transcripts for extracellular matrix proteins. Some genes not previously implicated in muscle atrophy were dramatically up-regulated (lipin, metallothionein, AMP deaminase, RNA helicase-related protein, TG interacting factor) and several growth-related mRNAs were down-regulated (P311, JUN, IGF-1-BP5). Thus, different types of muscle atrophy share a common transcriptional program that is activated in many systemic diseases.