The Experts below are selected from a list of 63 Experts worldwide ranked by ideXlab platform
J. T. R. Fitzsimons - One of the best experts on this subject based on the ideXlab platform.
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increased sodium appetite stimulates c fos expression in the organum vasculosum of the lamina terminalis
Neuroscience, 1997Co-Authors: J. M. Lane, J Herbert, J. T. R. FitzsimonsAbstract:Abstract The relation between c-fos expression in the forebrain of Lister hooded rats and water and NaCl intakes was examined in response to systemic injection of angiotensin II, Desoxycorticosterone, angiotensin II and Desoxycorticosterone together, frusemide or low sodium diet, all treatments that induce a sodium appetite. Angiotensin II (1 mg/kg subcutaneously) caused significant increases in the 1-h intakes of water and 1.8% NaCl compared to controls, the effect on water intake being the greater. There was a similar increase in NaCl intake after four days' treatment with Desoxycorticosterone (20 mg pellet subcutaneously) but water intake was not increased. The NaCl intake of rats given angiotensin II following Desoxycorticosterone treatment was approximately the sum of the intakes after angiotensin II or Desoxycorticosterone alone, but the water intake was slightly less than after angiotensin II alone. Frusemide pretreatment (4 mg/kg subcutaneously) caused an NaCl intake similar to that following angiotensin II and Desoxycorticosterone but water intake was little affected. Low dietary sodium also increased salt appetite, as expected. These treatments were repeated in rats that were not allowed to drink NaCl, after which the brains were processed for c-fos immunocytochemistry. This showed intense staining of the subfornical organ, median preoptic nucleus, organum vasculosum of the laminal terminalis, paraventricular nucleus and supraoptic nucleus after subcutanous angiotensin II. Animals given angiotensin II following Desoxycorticosterone pretreatment showed patterns of c-fos expression that did not differ from those of angiotensin II alone. Treatment with Desoxycorticosterone alone produced intense staining in the organum vasculosum of the laminal terminalis and some staining in the median preoptic nucleus. Frusemide gave a similar pattern of staining to Desoxycorticosterone, stimulating c-fos expression in the same regions but to a lesser extent. A low salt diet resulted in increased c-fos expression only in the organum vasculosum of the laminal terminalis. Therefore, five different treatments that induced increased sodium appetite evoked distinct patterns of c-fos expression in the anteroventral region of the third ventricle of the rat forebrain. Since the common feature was induction of c-fos in the organum vasculosum of the laminal terminalis, these results suggest a key role for this structure in the development of increased sodium appetite.
J. M. Lane - One of the best experts on this subject based on the ideXlab platform.
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increased sodium appetite stimulates c fos expression in the organum vasculosum of the lamina terminalis
Neuroscience, 1997Co-Authors: J. M. Lane, J Herbert, J. T. R. FitzsimonsAbstract:Abstract The relation between c-fos expression in the forebrain of Lister hooded rats and water and NaCl intakes was examined in response to systemic injection of angiotensin II, Desoxycorticosterone, angiotensin II and Desoxycorticosterone together, frusemide or low sodium diet, all treatments that induce a sodium appetite. Angiotensin II (1 mg/kg subcutaneously) caused significant increases in the 1-h intakes of water and 1.8% NaCl compared to controls, the effect on water intake being the greater. There was a similar increase in NaCl intake after four days' treatment with Desoxycorticosterone (20 mg pellet subcutaneously) but water intake was not increased. The NaCl intake of rats given angiotensin II following Desoxycorticosterone treatment was approximately the sum of the intakes after angiotensin II or Desoxycorticosterone alone, but the water intake was slightly less than after angiotensin II alone. Frusemide pretreatment (4 mg/kg subcutaneously) caused an NaCl intake similar to that following angiotensin II and Desoxycorticosterone but water intake was little affected. Low dietary sodium also increased salt appetite, as expected. These treatments were repeated in rats that were not allowed to drink NaCl, after which the brains were processed for c-fos immunocytochemistry. This showed intense staining of the subfornical organ, median preoptic nucleus, organum vasculosum of the laminal terminalis, paraventricular nucleus and supraoptic nucleus after subcutanous angiotensin II. Animals given angiotensin II following Desoxycorticosterone pretreatment showed patterns of c-fos expression that did not differ from those of angiotensin II alone. Treatment with Desoxycorticosterone alone produced intense staining in the organum vasculosum of the laminal terminalis and some staining in the median preoptic nucleus. Frusemide gave a similar pattern of staining to Desoxycorticosterone, stimulating c-fos expression in the same regions but to a lesser extent. A low salt diet resulted in increased c-fos expression only in the organum vasculosum of the laminal terminalis. Therefore, five different treatments that induced increased sodium appetite evoked distinct patterns of c-fos expression in the anteroventral region of the third ventricle of the rat forebrain. Since the common feature was induction of c-fos in the organum vasculosum of the laminal terminalis, these results suggest a key role for this structure in the development of increased sodium appetite.
J Herbert - One of the best experts on this subject based on the ideXlab platform.
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increased sodium appetite stimulates c fos expression in the organum vasculosum of the lamina terminalis
Neuroscience, 1997Co-Authors: J. M. Lane, J Herbert, J. T. R. FitzsimonsAbstract:Abstract The relation between c-fos expression in the forebrain of Lister hooded rats and water and NaCl intakes was examined in response to systemic injection of angiotensin II, Desoxycorticosterone, angiotensin II and Desoxycorticosterone together, frusemide or low sodium diet, all treatments that induce a sodium appetite. Angiotensin II (1 mg/kg subcutaneously) caused significant increases in the 1-h intakes of water and 1.8% NaCl compared to controls, the effect on water intake being the greater. There was a similar increase in NaCl intake after four days' treatment with Desoxycorticosterone (20 mg pellet subcutaneously) but water intake was not increased. The NaCl intake of rats given angiotensin II following Desoxycorticosterone treatment was approximately the sum of the intakes after angiotensin II or Desoxycorticosterone alone, but the water intake was slightly less than after angiotensin II alone. Frusemide pretreatment (4 mg/kg subcutaneously) caused an NaCl intake similar to that following angiotensin II and Desoxycorticosterone but water intake was little affected. Low dietary sodium also increased salt appetite, as expected. These treatments were repeated in rats that were not allowed to drink NaCl, after which the brains were processed for c-fos immunocytochemistry. This showed intense staining of the subfornical organ, median preoptic nucleus, organum vasculosum of the laminal terminalis, paraventricular nucleus and supraoptic nucleus after subcutanous angiotensin II. Animals given angiotensin II following Desoxycorticosterone pretreatment showed patterns of c-fos expression that did not differ from those of angiotensin II alone. Treatment with Desoxycorticosterone alone produced intense staining in the organum vasculosum of the laminal terminalis and some staining in the median preoptic nucleus. Frusemide gave a similar pattern of staining to Desoxycorticosterone, stimulating c-fos expression in the same regions but to a lesser extent. A low salt diet resulted in increased c-fos expression only in the organum vasculosum of the laminal terminalis. Therefore, five different treatments that induced increased sodium appetite evoked distinct patterns of c-fos expression in the anteroventral region of the third ventricle of the rat forebrain. Since the common feature was induction of c-fos in the organum vasculosum of the laminal terminalis, these results suggest a key role for this structure in the development of increased sodium appetite.
Yoshio Igarashi - One of the best experts on this subject based on the ideXlab platform.
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Neonatal Serum Deoxycorticosterone Sulfate Levels in Congenital Adrenal Hyperplasia due to 11β-Hydroxylase Deficiency
Clinical Pediatric Endocrinology, 1993Co-Authors: Akira Endoh, Akira Kubota, Haruo Ogawa, Yoshio IgarashiAbstract:Recent studies have demonstrated that deoxycorticosterone sulfate can be formed at extra-adrenal sites, but its actual origin and role are not yet clear. The present study was undertaken to elucidate the origin of deoxycorticosterone sulfate and the usefulness of this steroid for the diagnosis of 11β-hydroxylase deficiency in the early neonatal period. We measured serum deoxycorticosterone sulfate levels during glucocorticoid therapy in an infant with 11β-hydroxylase deficiency. Before therapy, the serum deoxycorticosterone sulfate concentration at 6 days of life was higher than normal. Following glucocorticoid therapy, the serum deoxycorticosterone sulfate concentration showed a marked and dose-dependent suppression, as did the serum deoxycorticosterone and 11-deoxycortisol levels. These findings suggest that serum deoxycorticosterone sulfate can be used as another specific indicator for the diagnosis of 11β-hydroxylase deficiency in neonates, and that the adrenal glands may play an important role in neonatal deoxycorticosterone sulfate production under the control of ACTH.
Akira Endoh - One of the best experts on this subject based on the ideXlab platform.
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Neonatal Serum Deoxycorticosterone Sulfate Levels in Congenital Adrenal Hyperplasia due to 11β-Hydroxylase Deficiency
Clinical Pediatric Endocrinology, 1993Co-Authors: Akira Endoh, Akira Kubota, Haruo Ogawa, Yoshio IgarashiAbstract:Recent studies have demonstrated that deoxycorticosterone sulfate can be formed at extra-adrenal sites, but its actual origin and role are not yet clear. The present study was undertaken to elucidate the origin of deoxycorticosterone sulfate and the usefulness of this steroid for the diagnosis of 11β-hydroxylase deficiency in the early neonatal period. We measured serum deoxycorticosterone sulfate levels during glucocorticoid therapy in an infant with 11β-hydroxylase deficiency. Before therapy, the serum deoxycorticosterone sulfate concentration at 6 days of life was higher than normal. Following glucocorticoid therapy, the serum deoxycorticosterone sulfate concentration showed a marked and dose-dependent suppression, as did the serum deoxycorticosterone and 11-deoxycortisol levels. These findings suggest that serum deoxycorticosterone sulfate can be used as another specific indicator for the diagnosis of 11β-hydroxylase deficiency in neonates, and that the adrenal glands may play an important role in neonatal deoxycorticosterone sulfate production under the control of ACTH.