The Experts below are selected from a list of 210 Experts worldwide ranked by ideXlab platform
Joseph G Verbalis - One of the best experts on this subject based on the ideXlab platform.
-
control of brain volume during Hypoosmolality and hyperosmolality
Advances in Experimental Medicine and Biology, 2006Co-Authors: Joseph G VerbalisAbstract:Multiple studies over several decades have provided evidence that both electrolytes and organic osmolytes play crucial roles in regulating brain volume, both during increases as well as during decreases in extracellular fluid osmolality. In both situations, rapidly, and however, changes in brain electrolyte contents appear to occur more represent the first line of defense of brain volume during acute perturbations of body fluid tonicity, while organic osmolytes allow adaptation to more chronic perturbations. For both hyperosmolality and Hypoosmolality, the rate of development of the disorder is an important determinant of neurological morbidity and mortality, since sufficiently rapid changes in tonicity can exceed the brain's capacity to regulate its volume leading to more severe degrees of brain edema or dehydration. Recovery from both hyper- and Hypoosmolality requires reversal of the adaptive processes that enabled regulation of brain volume in response to the initial insult. However, adaptation and recovery are not symmetrical processes. Marked differences occur in the speed with which the brain is able to lose or to reaccumulate different types of solutes after recovery from chronic disturbances of body fluid tonicity. In general, accumulation, or reaccumulation, of organic solutes by brain tissue is a much slower process than volume regulatory losses of such solutes. As with the adaptation process, the rate of recovery is an important determinant of subsequent morbidity and mortality, since rapid corrections of osmolality can also exceed the capacity of the brain to readjust its solute content, and consequently its volume, back to normal levels. Whether or not transient excesses or deficiencies of either electrolytes or specific organic osmolytes in brain intracellular or extracellular fluid contribute to functional disturbances independently of changes in brain volume is an intriguing question that has not been sufficiently evaluated. Also remaining to be answered are questions regarding other physiological, pathophysiological, and pharmacological factors that either impair or enhance volume regulatory processes, and thereby modify the neurological manifestations accompanying disorders of body fluid osmolality in humans. Finally, a complete understanding of the cellular mechanisms underlying adaptation to and deadaptation from acute and chronic perturbations of body osmolality will be essential to design the most enlightened, and therefore appropriate, treatments for these disorders.
-
regulation of gene expression in magnocellular neurons in rat supraoptic nucleus during sustained Hypoosmolality
Endocrinology, 2005Co-Authors: Noriko Mutsuga, Joseph G Verbalis, Tal Shahar, Charlie C Xiang, Michael J Brownstein, Harold GainerAbstract:Hypoosmolality produces a dramatic inhibition of vasopressin (VP) and oxytocin gene expression in the supraoptic nucleus (SON). This study examines the effect of sustained Hypoosmolality on global gene expression in the oxytocin and VP magnocellular neurons of the hypothalamo-neurohypophysial system, to identify genes associated with the magnocellular neuron’s adaptation to this physiological condition. Using laser microdissection of the SON, T7-based linear amplification of its RNA, and a 35,319-element cDNA microarray, we compare gene expression profiles between SONs in normoosmolar (control), 1-desamino-[8-d-arginine]-VP-treated normoosmolar, and hypoosmolar rats. We found 4959 genes with statistically significant differences in expression between normosmolar control and the hypoosmolar SONs, with 1564 of these differing in expression by more than 2-fold. These genes serve a wide variety of functions, and most were up-regulated in gene expression in hypoosmolar compared with control SONs. Of these, 90 ...
-
chronic Hypoosmolality induces a selective decrease in magnocellular neurone soma and nuclear size in the rat hypothalamic supraoptic nucleus
Journal of Neuroendocrinology, 2001Co-Authors: Eric Glasgow, Joseph G Verbalis, T Murase, Harold GaineAbstract:The magnocellular neurones of the hypothalamo-neurohypophysial system (HNS) play a vital role in the maintenance of body homeostasis by regulating oxytocin (OT) and vasopressin (VP) secretion from the posterior pituitary. During hyperosmolality, OT and VP mRNA levels are known to increase by approximately two-fold, whereas during chronic Hypoosmolality, OT and VP mRNA levels decrease to approximately 10-20% of basal levels. In these studies, we evaluated changes in cell size associated with these physiological conditions. Cell and nuclear sizes of neurones in the supraoptic nucleus (SON), the nucleus of the lateral olfactory tract (LOT) and the medial habenular nucleus (MHB) were measured from neurones identified by in situ hybridization histochemistry for beta(III)-tubulin mRNA, and measurements were made from OT and AVP magnocellular neurones in the SON after phenotypic identification by immunohistochemistry. Under hypoosmolar conditions, the cell and nuclear sizes of OT and VP magnocellular neurones decreased to approximately 60% of basal values, whereas cell and nuclear sizes of OT and VP neurones in hyperosmolar rats increased to approximately 170% of basal values. In contrast, neither hyperosmolality, nor Hypoosmolality significantly affected cell and nuclear sizes in the LOT and MHB. These results confirm previous studies that showed that magnocellular neurones increase cell size in response to hyperosmolar conditions and, for the first time, demonstrate a marked decrease in cell size in the SON in response to chronic hypoosmolar conditions. These dramatic changes in cell and nuclear size directly parallel changes in OT and VP gene expression in the magnocellular neurones of the SON and, consequently, are consistent with the pronounced bidirectional changes in gene expression and cellular activity found during these osmotic perturbations. Our results therefore support the concept of global alterations in the synthetic activity of magnocellular OT and AVP neurones in response to extracellular osmolality.
Ulrich Kelle - One of the best experts on this subject based on the ideXlab platform.
-
effects of Hypoosmolality on whole body lipolysis in man
Metabolism-clinical and Experimental, 1999Co-Authors: Stefa Ilz, Ronald Ninnis, Ulrich KelleAbstract:Abstract Changes in extracellular osmolality, and thus in the cellular hydration state, appear to directly influence cell metabolism. The metabolic changes associated with cell swelling are inhibition of glycogenolysis, glycolysis, and proteolysis. Recent studies in our laboratory demonstrated diminished whole-body protein breakdown in humans during an acute hypoosmolar state. Because of the close interrelationship between carbohydrate and fat metabolism, we speculated that adipose tissue lipolysis and fatty acid oxidation are regulated by changes in extracellular osmolality. Therefore, we investigated the effect of artificially induced Hypoosmolality on whole-body lipolysis and fat oxidation in seven healthy young men. Hypoosmolality was induced by intravenous administration of desmopressin, liberal ingestion of water, and infusion of hypotonic (0.45%) saline solution. Lipolysis was assessed by a stable-isotope method (2-[13C]-glycerol infusion). The glycerol rate of appearance (Ra), reflecting whole-body lipolysis, was higher under hypoosmolar compared with isoosmolar conditions (2.35 ± 0.40 v 1.68 ± 0.21 μmol/kg/min, P = .03). This was even more pronounced when lipolysis was suppressed during hyperinsulinemia and euglycemic clamping (0.90 ± 0.08 v 0.61 ± 0.03 μmol/kg/min, P = .002). However, plasma free fatty acid (FFA), glycerol, ketone body, insulin, and glucagon concentrations and carbohydrate and lipid oxidation measured by indirect calorimetry were not significantly altered by Hypoosmolality. Plasma norepinephrine concentrations were lower under hypoosmolar conditions (P
-
effects of hyper and Hypoosmolality on whole body protein and glucose kinetics in humans
American Journal of Physiology-endocrinology and Metabolism, 1999Co-Authors: Kaspa Erneis, Ronald Ninnis, Diete Haussinge, Ulrich KelleAbstract:To investigate the effect of acute changes of extracellular osmolality on whole body protein and glucose metabolism, we studied 10 male subjects during three conditions: hyperosmolality was induced...
Harold Gainer - One of the best experts on this subject based on the ideXlab platform.
-
regulation of gene expression in magnocellular neurons in rat supraoptic nucleus during sustained Hypoosmolality
Endocrinology, 2005Co-Authors: Noriko Mutsuga, Joseph G Verbalis, Tal Shahar, Charlie C Xiang, Michael J Brownstein, Harold GainerAbstract:Hypoosmolality produces a dramatic inhibition of vasopressin (VP) and oxytocin gene expression in the supraoptic nucleus (SON). This study examines the effect of sustained Hypoosmolality on global gene expression in the oxytocin and VP magnocellular neurons of the hypothalamo-neurohypophysial system, to identify genes associated with the magnocellular neuron’s adaptation to this physiological condition. Using laser microdissection of the SON, T7-based linear amplification of its RNA, and a 35,319-element cDNA microarray, we compare gene expression profiles between SONs in normoosmolar (control), 1-desamino-[8-d-arginine]-VP-treated normoosmolar, and hypoosmolar rats. We found 4959 genes with statistically significant differences in expression between normosmolar control and the hypoosmolar SONs, with 1564 of these differing in expression by more than 2-fold. These genes serve a wide variety of functions, and most were up-regulated in gene expression in hypoosmolar compared with control SONs. Of these, 90 ...
Jorge Warberg - One of the best experts on this subject based on the ideXlab platform.
-
selective inhibition of magnocellular vasopressin neurons by Hypoosmolality effect on histamine and stress induced secretion of adrenocorticotropin and prolactin
Neuroendocrinology, 1998Co-Authors: Andreas Kjae, Ulrich Knigge, Henrik L Jorgense, Jorge WarbergAbstract:We investigated the effect of selective inhibition of magnocellular arginine vasopressin (AVP) and oxytocin neurons on histamine (HA)- and restraint-stress-induced adrenocorticotropin (ACTH) and prolactin (PRL) secretion in conscious male rats. The inhibition of magnocellular neurons was obtained by inducing chronic Hypoosmolality via continuous exposure of the rats to the AVP V2 receptor agonist 1-deamino(8-D-arginine)vasopressin (DDAVP) which was released from osmotic pumps implanted subcutaneously. In DDAVP-treated rats, plasma osmolality and sodium concentration were 273 mosm/l and 130 mmol/l, respectively. In control rats, the corresponding values were 291 mosm/l and 139 mmol/l. HA (270 nmol) administered intracerebroventricularly or 5 min of restraint stress stimulated ACTH and PRL secretion 4- to 11-fold in normoosmolar rats. In hypoosmolar rats, the HA-induced ACTH response was inhibited more than 40% whereas the restraint-stress-induced ACTH response was unaffected. Conversely, the PRL response to HA in hypoosmolar rats was unaffected whereas the PRL response to restraint stress was inhibited by 40%. In summary, chronic Hypoosmolality inhibits HA-induced ACTH and restraint-stress-induced PRL secretion indicating involvement of magnocellular AVP in these responses.
Harold Gaine - One of the best experts on this subject based on the ideXlab platform.
-
chronic Hypoosmolality induces a selective decrease in magnocellular neurone soma and nuclear size in the rat hypothalamic supraoptic nucleus
Journal of Neuroendocrinology, 2001Co-Authors: Eric Glasgow, Joseph G Verbalis, T Murase, Harold GaineAbstract:The magnocellular neurones of the hypothalamo-neurohypophysial system (HNS) play a vital role in the maintenance of body homeostasis by regulating oxytocin (OT) and vasopressin (VP) secretion from the posterior pituitary. During hyperosmolality, OT and VP mRNA levels are known to increase by approximately two-fold, whereas during chronic Hypoosmolality, OT and VP mRNA levels decrease to approximately 10-20% of basal levels. In these studies, we evaluated changes in cell size associated with these physiological conditions. Cell and nuclear sizes of neurones in the supraoptic nucleus (SON), the nucleus of the lateral olfactory tract (LOT) and the medial habenular nucleus (MHB) were measured from neurones identified by in situ hybridization histochemistry for beta(III)-tubulin mRNA, and measurements were made from OT and AVP magnocellular neurones in the SON after phenotypic identification by immunohistochemistry. Under hypoosmolar conditions, the cell and nuclear sizes of OT and VP magnocellular neurones decreased to approximately 60% of basal values, whereas cell and nuclear sizes of OT and VP neurones in hyperosmolar rats increased to approximately 170% of basal values. In contrast, neither hyperosmolality, nor Hypoosmolality significantly affected cell and nuclear sizes in the LOT and MHB. These results confirm previous studies that showed that magnocellular neurones increase cell size in response to hyperosmolar conditions and, for the first time, demonstrate a marked decrease in cell size in the SON in response to chronic hypoosmolar conditions. These dramatic changes in cell and nuclear size directly parallel changes in OT and VP gene expression in the magnocellular neurones of the SON and, consequently, are consistent with the pronounced bidirectional changes in gene expression and cellular activity found during these osmotic perturbations. Our results therefore support the concept of global alterations in the synthetic activity of magnocellular OT and AVP neurones in response to extracellular osmolality.