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Luis G Melo - One of the best experts on this subject based on the ideXlab platform.

  • regulation of sodium calcium and vitamin d metabolism in dahl rats on a high salt low potassium diet genetic and neural influences
    Clinical and Experimental Pharmacology and Physiology, 2000
    Co-Authors: Xiaoyan Wu, Reinhold Vieth, Susan Milojevic, H Sonnenberg, Luis G Melo
    Abstract:

    1. A dietary combination of high salt and low potassium (HSLK) exacerbates hypertension in Dahl salt-sensitive (DS) rats and renders previously normotensive Dahl salt-resistant (DR) rats hypertensive. In both strains, the severity of hypertension correlates with urinary calcium loss. However, the magnitude of excretory calcium losses is significantly greater in DS rats and is potentiated by Chemical Sympathectomy in both strains. 2. We hypothesized that a defect in vitamin D metabolism may underlie the observed strain-dependent differences in calcium balance.

  • regulation of sodium calcium and vitamin d metabolism in dahl rats on a high salt low potassium diet genetic and neural influences
    Clinical and Experimental Pharmacology and Physiology, 2000
    Co-Authors: Reinhold Vieth, Susan Milojevic, H Sonnenberg, Luis G Melo
    Abstract:

    1. A dietary combination of high salt and low potassium (HSLK) exacerbates hypertension in Dahl salt-sensitive (DS) rats and renders previously normotensive Dahl salt-resistant (DR) rats hypertensive. In both strains, the severity of hypertension correlates with urinary calcium loss. However, the magnitude of excretory calcium losses is significantly greater in DS rats and is potentiated by Chemical Sympathectomy in both strains. 2. We hypothesized that a defect in vitamin D metabolism may underlie the observed strain-dependent differences in calcium balance. 3. Arterial blood pressure (ABP), water and mineral balance and serum concentrations of 1,25-dihydroxyvitamin D3 (1,25(OH)2 D3) and 25-hydroxyvitamin D3 (25(OH)D3) were measured in intact and Chemically sympathectomized (6-hydroxydopamine; 6-OHDA) DS and DR rats after 8 weeks on a HSLK diet. 4. Chronic ingestion of this diet resulted in marked and moderate levels of hypertension in DS and DR rats, respectively. The hypertension was abated and eliminated by 6-OHDA in the DS and DR strains, respectively. Independent of treatment, DS rats had significantly higher urinary excretion of calcium and reduced intestinal absorption of the ion compared with DR rats. The DS rats had significantly higher serum levels of 1,25(OH)2 D3 and markedly lower serum levels of 25(OH)D3 than DR rats. Chemical Sympathectomy tended to increase 1,25(OH)2 D3 and to decrease 25(OH)D3 levels in both strains. 5. These data indicate a genetic difference in vitamin D metabolism between DS and DR rats. The abnormally elevated levels of 1,25(OH)2 D3 in DS rats may be an appropriate compensatory response to excessive excretory calcium loss and reduced target organ sensitivity to the hormone and may, maladaptively, directly contribute to hypertension, by stimulating vascular smooth muscle contractility.

Monica M Brauer - One of the best experts on this subject based on the ideXlab platform.

  • guanethidine on developing cholinergic nerves of the rat uterus effects of infantile prepubertal chronic estrogen treatment and Chemical Sympathectomy with
    2013
    Co-Authors: Analia Richeri, Lorena Viettro, Rebeca Chavezgenaro, Geoffrey Burnstock, Timothy Cowen, Monica M Brauer
    Abstract:

    SUMMARY The innervation of the uterus is remarkable in that it exhibits physiologicalchanges in response to altered levels in the circulating levels of sex hormones. Previousstudies by our group showed that chronic administration of estrogen to rats during the in-fantile/prepubertal period provoked, at 28 days of age, an almost complete loss of norepi-nephrine-labeled sympathetic nerves, similar to that observed in late pregnancy. It is notknown, however, whether early exposure to estrogen affects uterine cholinergic nerves.Similarly, it is not known to what extent development and estrogen-induced responses inthe uterine cholinergic innervation are affected by the absence of sympathetic nerves. Toaddress this question, in this study we analyzed the effects of infantile/prepubertal chronicestrogen treatment, chronic Chemical Sympathectomy with guanethidine, and combinedSympathectomy and chronic estrogen treatment on developing cholinergic nerves of therat uterus. Cholinergic nerves were visualized using a combination of acetylcholinesterasehistochemistry and the immunohistoChemical demonstration of the vesicular acetylcholinetransporter (VAChT). After chronic estrogen treatment, a well-developed plexus of cholin-ergic nerves was observed in the uterus. Quantitative studies showed that chronic exposureto estrogen induced contrasting responses in uterine cholinergic nerves, increasing thedensity of large and medium-sized nerve bundles and reducing the intercept density offine fibers providing myometrial and perivascular innervation. Estrogen-induced changesin the uterine cholinergic innervation did not appear to result from the absence/impair-ment of sympathetic nerves, because Sympathectomy did not mimic the effects producedby estrogen. Estrogen-induced responses in parasympathetic nerves are discussed, consid-ering the direct effects of estrogen on neurons and on changes in neuron–targetinteractions.

  • effects of infantile prepubertal chronic estrogen treatment and Chemical Sympathectomy with guanethidine on developing cholinergic nerves of the rat uterus
    Journal of Histochemistry and Cytochemistry, 2002
    Co-Authors: Analia Richeri, Lorena Viettro, Rebeca Chavezgenaro, Geoffrey Burnstock, Timothy Cowen, Monica M Brauer
    Abstract:

    The innervation of the uterus is remarkable in that it exhibits physiological changes in response to altered levels in the circulating levels of sex hormones. Previous studies by our group showed that chronic administration of estrogen to rats during the infantile/prepubertal period provoked, at 28 days of age, an almost complete loss of norepinephrine-labeled sympathetic nerves, similar to that observed in late pregnancy. It is not known, however, whether early exposure to estrogen affects uterine cholinergic nerves. Similarly, it is not known to what extent development and estrogen-induced responses in the uterine cholinergic innervation are affected by the absence of sympathetic nerves. To address this question, in this study we analyzed the effects of infantile/prepubertal chronic estrogen treatment, chronic Chemical Sympathectomy with guanethidine, and combined Sympathectomy and chronic estrogen treatment on developing cholinergic nerves of the rat uterus. Cholinergic nerves were visualized using a combination of acetylcholinesterase histochemistry and the immunohistoChemical demonstration of the vesicular acetylcholine transporter (VAChT). After chronic estrogen treatment, a well-developed plexus of cholinergic nerves was observed in the uterus. Quantitative studies showed that chronic exposure to estrogen induced contrasting responses in uterine cholinergic nerves, increasing the density of large and medium-sized nerve bundles and reducing the intercept density of fine fibers providing myometrial and perivascular innervation. Estrogen-induced changes in the uterine cholinergic innervation did not appear to result from the absence/impairment of sympathetic nerves, because Sympathectomy did not mimic the effects produced by estrogen. Estrogen-induced responses in parasympathetic nerves are discussed, considering the direct effects of estrogen on neurons and on changes in neuron-target interactions.

Reinhold Vieth - One of the best experts on this subject based on the ideXlab platform.

  • regulation of sodium calcium and vitamin d metabolism in dahl rats on a high salt low potassium diet genetic and neural influences
    Clinical and Experimental Pharmacology and Physiology, 2000
    Co-Authors: Xiaoyan Wu, Reinhold Vieth, Susan Milojevic, H Sonnenberg, Luis G Melo
    Abstract:

    1. A dietary combination of high salt and low potassium (HSLK) exacerbates hypertension in Dahl salt-sensitive (DS) rats and renders previously normotensive Dahl salt-resistant (DR) rats hypertensive. In both strains, the severity of hypertension correlates with urinary calcium loss. However, the magnitude of excretory calcium losses is significantly greater in DS rats and is potentiated by Chemical Sympathectomy in both strains. 2. We hypothesized that a defect in vitamin D metabolism may underlie the observed strain-dependent differences in calcium balance.

  • regulation of sodium calcium and vitamin d metabolism in dahl rats on a high salt low potassium diet genetic and neural influences
    Clinical and Experimental Pharmacology and Physiology, 2000
    Co-Authors: Reinhold Vieth, Susan Milojevic, H Sonnenberg, Luis G Melo
    Abstract:

    1. A dietary combination of high salt and low potassium (HSLK) exacerbates hypertension in Dahl salt-sensitive (DS) rats and renders previously normotensive Dahl salt-resistant (DR) rats hypertensive. In both strains, the severity of hypertension correlates with urinary calcium loss. However, the magnitude of excretory calcium losses is significantly greater in DS rats and is potentiated by Chemical Sympathectomy in both strains. 2. We hypothesized that a defect in vitamin D metabolism may underlie the observed strain-dependent differences in calcium balance. 3. Arterial blood pressure (ABP), water and mineral balance and serum concentrations of 1,25-dihydroxyvitamin D3 (1,25(OH)2 D3) and 25-hydroxyvitamin D3 (25(OH)D3) were measured in intact and Chemically sympathectomized (6-hydroxydopamine; 6-OHDA) DS and DR rats after 8 weeks on a HSLK diet. 4. Chronic ingestion of this diet resulted in marked and moderate levels of hypertension in DS and DR rats, respectively. The hypertension was abated and eliminated by 6-OHDA in the DS and DR strains, respectively. Independent of treatment, DS rats had significantly higher urinary excretion of calcium and reduced intestinal absorption of the ion compared with DR rats. The DS rats had significantly higher serum levels of 1,25(OH)2 D3 and markedly lower serum levels of 25(OH)D3 than DR rats. Chemical Sympathectomy tended to increase 1,25(OH)2 D3 and to decrease 25(OH)D3 levels in both strains. 5. These data indicate a genetic difference in vitamin D metabolism between DS and DR rats. The abnormally elevated levels of 1,25(OH)2 D3 in DS rats may be an appropriate compensatory response to excessive excretory calcium loss and reduced target organ sensitivity to the hormone and may, maladaptively, directly contribute to hypertension, by stimulating vascular smooth muscle contractility.

Analia Richeri - One of the best experts on this subject based on the ideXlab platform.

  • guanethidine on developing cholinergic nerves of the rat uterus effects of infantile prepubertal chronic estrogen treatment and Chemical Sympathectomy with
    2013
    Co-Authors: Analia Richeri, Lorena Viettro, Rebeca Chavezgenaro, Geoffrey Burnstock, Timothy Cowen, Monica M Brauer
    Abstract:

    SUMMARY The innervation of the uterus is remarkable in that it exhibits physiologicalchanges in response to altered levels in the circulating levels of sex hormones. Previousstudies by our group showed that chronic administration of estrogen to rats during the in-fantile/prepubertal period provoked, at 28 days of age, an almost complete loss of norepi-nephrine-labeled sympathetic nerves, similar to that observed in late pregnancy. It is notknown, however, whether early exposure to estrogen affects uterine cholinergic nerves.Similarly, it is not known to what extent development and estrogen-induced responses inthe uterine cholinergic innervation are affected by the absence of sympathetic nerves. Toaddress this question, in this study we analyzed the effects of infantile/prepubertal chronicestrogen treatment, chronic Chemical Sympathectomy with guanethidine, and combinedSympathectomy and chronic estrogen treatment on developing cholinergic nerves of therat uterus. Cholinergic nerves were visualized using a combination of acetylcholinesterasehistochemistry and the immunohistoChemical demonstration of the vesicular acetylcholinetransporter (VAChT). After chronic estrogen treatment, a well-developed plexus of cholin-ergic nerves was observed in the uterus. Quantitative studies showed that chronic exposureto estrogen induced contrasting responses in uterine cholinergic nerves, increasing thedensity of large and medium-sized nerve bundles and reducing the intercept density offine fibers providing myometrial and perivascular innervation. Estrogen-induced changesin the uterine cholinergic innervation did not appear to result from the absence/impair-ment of sympathetic nerves, because Sympathectomy did not mimic the effects producedby estrogen. Estrogen-induced responses in parasympathetic nerves are discussed, consid-ering the direct effects of estrogen on neurons and on changes in neuron–targetinteractions.

  • effects of infantile prepubertal chronic estrogen treatment and Chemical Sympathectomy with guanethidine on developing cholinergic nerves of the rat uterus
    Journal of Histochemistry and Cytochemistry, 2002
    Co-Authors: Analia Richeri, Lorena Viettro, Rebeca Chavezgenaro, Geoffrey Burnstock, Timothy Cowen, Monica M Brauer
    Abstract:

    The innervation of the uterus is remarkable in that it exhibits physiological changes in response to altered levels in the circulating levels of sex hormones. Previous studies by our group showed that chronic administration of estrogen to rats during the infantile/prepubertal period provoked, at 28 days of age, an almost complete loss of norepinephrine-labeled sympathetic nerves, similar to that observed in late pregnancy. It is not known, however, whether early exposure to estrogen affects uterine cholinergic nerves. Similarly, it is not known to what extent development and estrogen-induced responses in the uterine cholinergic innervation are affected by the absence of sympathetic nerves. To address this question, in this study we analyzed the effects of infantile/prepubertal chronic estrogen treatment, chronic Chemical Sympathectomy with guanethidine, and combined Sympathectomy and chronic estrogen treatment on developing cholinergic nerves of the rat uterus. Cholinergic nerves were visualized using a combination of acetylcholinesterase histochemistry and the immunohistoChemical demonstration of the vesicular acetylcholine transporter (VAChT). After chronic estrogen treatment, a well-developed plexus of cholinergic nerves was observed in the uterus. Quantitative studies showed that chronic exposure to estrogen induced contrasting responses in uterine cholinergic nerves, increasing the density of large and medium-sized nerve bundles and reducing the intercept density of fine fibers providing myometrial and perivascular innervation. Estrogen-induced changes in the uterine cholinergic innervation did not appear to result from the absence/impairment of sympathetic nerves, because Sympathectomy did not mimic the effects produced by estrogen. Estrogen-induced responses in parasympathetic nerves are discussed, considering the direct effects of estrogen on neurons and on changes in neuron-target interactions.

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

  • regulation of sodium calcium and vitamin d metabolism in dahl rats on a high salt low potassium diet genetic and neural influences
    Clinical and Experimental Pharmacology and Physiology, 2000
    Co-Authors: Xiaoyan Wu, Reinhold Vieth, Susan Milojevic, H Sonnenberg, Luis G Melo
    Abstract:

    1. A dietary combination of high salt and low potassium (HSLK) exacerbates hypertension in Dahl salt-sensitive (DS) rats and renders previously normotensive Dahl salt-resistant (DR) rats hypertensive. In both strains, the severity of hypertension correlates with urinary calcium loss. However, the magnitude of excretory calcium losses is significantly greater in DS rats and is potentiated by Chemical Sympathectomy in both strains. 2. We hypothesized that a defect in vitamin D metabolism may underlie the observed strain-dependent differences in calcium balance.

  • regulation of sodium calcium and vitamin d metabolism in dahl rats on a high salt low potassium diet genetic and neural influences
    Clinical and Experimental Pharmacology and Physiology, 2000
    Co-Authors: Reinhold Vieth, Susan Milojevic, H Sonnenberg, Luis G Melo
    Abstract:

    1. A dietary combination of high salt and low potassium (HSLK) exacerbates hypertension in Dahl salt-sensitive (DS) rats and renders previously normotensive Dahl salt-resistant (DR) rats hypertensive. In both strains, the severity of hypertension correlates with urinary calcium loss. However, the magnitude of excretory calcium losses is significantly greater in DS rats and is potentiated by Chemical Sympathectomy in both strains. 2. We hypothesized that a defect in vitamin D metabolism may underlie the observed strain-dependent differences in calcium balance. 3. Arterial blood pressure (ABP), water and mineral balance and serum concentrations of 1,25-dihydroxyvitamin D3 (1,25(OH)2 D3) and 25-hydroxyvitamin D3 (25(OH)D3) were measured in intact and Chemically sympathectomized (6-hydroxydopamine; 6-OHDA) DS and DR rats after 8 weeks on a HSLK diet. 4. Chronic ingestion of this diet resulted in marked and moderate levels of hypertension in DS and DR rats, respectively. The hypertension was abated and eliminated by 6-OHDA in the DS and DR strains, respectively. Independent of treatment, DS rats had significantly higher urinary excretion of calcium and reduced intestinal absorption of the ion compared with DR rats. The DS rats had significantly higher serum levels of 1,25(OH)2 D3 and markedly lower serum levels of 25(OH)D3 than DR rats. Chemical Sympathectomy tended to increase 1,25(OH)2 D3 and to decrease 25(OH)D3 levels in both strains. 5. These data indicate a genetic difference in vitamin D metabolism between DS and DR rats. The abnormally elevated levels of 1,25(OH)2 D3 in DS rats may be an appropriate compensatory response to excessive excretory calcium loss and reduced target organ sensitivity to the hormone and may, maladaptively, directly contribute to hypertension, by stimulating vascular smooth muscle contractility.