Role of plasma arginine vasopressin in the impaired water diuresis of isolated glucocorticoid deficiency in the rat

Role of plasma arginine vasopressin in the impaired water diuresis of isolated glucocorticoid deficiency in the rat. The role of antidiuretic hormone in the impaired water excretion of isolated glucocorticoid deficiency was investigated in the thyroxin-re-placed, anterior hypophysectomized rat. Hypophysectomized rats demonstrated marked impairment in the excretion of an oral water load (32 ± 4% vs. 94 ± 4%), plasma hypoosmolality (281 ± 2 vs. 289 ± 2 mOsm/kg), and hyponatremia (129 ± 1 vs. 140 ± 1 mEq/liter) compared to controls (all P < 0.001). These defects were associated with increased levels of plasma arginine vasopressin (3.05 ± 0.45 vs. 1.38 ± 0.11 pg/ml; P < 0.001). Following physiologic corticosterone replacement in hypophysectomized rats, the percentage of the water load excreted, free water clearance, plasma sodium, plasma osmolality, and circulating levels of plasma arginine vasopressin were all restored to control values. This correction of water diuresis occurred in the absence of changes in GFR or solute excretion. The defect in water excretion and the elevation of plasma arginine vasopressin could not be corrected by chronic extracellular volume expansion in the absence of glucocorticoid replacement. It is concluded that (a) increased secretion of vasopressin plays an important role in the impaired water diuresis of isolated glucorticoid deficiency; (b) physiologic corticosterone replacement corrects both the impaired water excretion and the increased secretion of vasopressin associated with glucocorticoid deficiency; and (c) a volume-independent nonosmotic stimulus to vasopressin secretion may be activated by the chronic absence of glucocorticoid hormones.Rôle de l'rginine vasopressine du plasma dans l'ncapacite de diluer l'urine au cours du déficit isolé en glucocorticoïdes chez le rat. Le rôle de l'hormone antidiurétique dans l'incapacité à diluer l'urine au cours du déficit isolé en glucocorticoïdes a été étudié chez des rats ayant subi une hypophysectomie antérieure et compensés par de la thyroxine. Les rats hypohysectomisés ont un déficit important de l'excrétion d'une charge en eau (32 ± 4% contre 94 ± 4%), une hypoosmolalité plasmatique (281 ± 2 contre 289 ± 2 mOsm/kg), et une hyponatrémie (129 ± 1 contre 140 ± 1 mEq/liter), par comparaison aux contrôles (P < 0,001). Ces modifications sont associées à des concentrations plasmatiques élevées d'arginine vasopressine (3,05 ± 0,45 contre 1,38 ± 0,11 pg/ml; P < 0,001). L'administration de corticostérone aux rats hypophysectomisés ramène aux valeurs contrôles le pourcentage de la charge d'eau excrétée, la clearance de l'eau libre, la natrémie, l'osmolalité plasmatique et la concentration circulante d'arginine vasopressine. Cette restauration de la diurèse aqueuse est observée en l'absence de modifications du débit de filtration glomérulaire ou du débit urinaire de substances dissoutes. Le déficit d'excrétion de l'eau et l'augmentation de l'arginine vasopressine du plasma ne peuvent pas être corrigés par une expansion chronique du volume extra-cellulaire en l'absence de traitement substitutif par les glucocorticoïdes. I1 est conclu que: (a) l'augmentation de la sécrétion de vasopressine joue un rôle important dans l'incapacité de diluer les urines observée au cours du déficit en glucocorticoïdes; (b) un traitement substitutif par des doses physiologiques de corticostérone corrige à la fois le déficit d'excrétion de l'eau et la sécrétion excessive de vasopressine associés au déficit en glucocorticoïdes; et (c) un stimulus, non osmotique et indépendant du volume extracellulaire, de la sécrétion de vasopressine peut être activé par l'absence chronique d'hormones glucocorticoïdes

Role of vasopressin in impaired water excretion in conscious rats with experimental cirrhosis

Role of vasopressin in impaired water excretion in conscious rats with experimental cirrhosis. The present study was undertaken to study the mechanism of impaired water excretion in experimental cirrhosis in the rat. Conscious rats in whom histologically proven cirrhosis was induced with carbon tetrachloride and phenobarbital were compared with control rats given phenobarbital alone. Impaired water excretion in experimental cirrhosis was verified by a basal hyponatremia (138 vs. 147 mEq/liter, P < 0.005) and an impaired excretion of water load (minimal urinary osmolality, 262 vs. 100 mOsm/kg; 58 vs. 102% of water load excreted, P < 0.001). To clarify the mechanism of this impaired water excretion, we measured glomerular filtration rate (GFR), renal blood flow (RBF), and vasopressin (VP) levels. In cirrhosis, GFR was normal but RBF was decreased (4.5 vs 6.8 ml/min/g, P < 0.01). VP levels were found to be higher in cirrhotic rats (1.61 vs. 0.71 pg/ml, P < 0.025). The significance of the impaired renal hemodynamics and the increase in VP was assessed by inducing cirrhosis in VP-free Brattle-boro (diabetes insipidus; DI) rats. Despite histologic, biochemical, and renal hemodynamic changes that were comparable to cirrhotic rats with an intact neurohypophysis, cirrhotic DI rats had no impairment in water excretion. To determine the cause of increased VP in experimental cirrhosis, we determined blood volume and systemic hemodynamics. Although plasma volume was greater in experimental cirrhosis (4.3 vs. 3.0 ml/100 g, P < 0.05), cirrhotic rats had a significantly lower peripheral resistance (0.37 vs. 0.42mm Hg/ml/min/kg, P < 0.05) and mean arterial pressure (104 vs. 120mm Hg, P < 0.001) than did control rats. These results document that experimental cirrhosis in the rat is associated with impaired renal water excretion in association with both abnormal renal hemodynamics and increased VP levels. The impaired water excretion, however, is solely VP mediated. The nonosmolar stimulus for VP release may be due to abnormal systemic hemodynamics.Rôle de la vasopressine dans l'altération de l'excrétion de l'eau par le rat conscient atteint de cirrhose expérimentale. Cette étude a été entreprise pour élucider le mécanisme de l'altération de l'excrétion de l'eau au cours de la cirrhose du rat. Des rats conscients chez lesquels une cirrhose prouvée histologiquement a été induite par le tétrachlorure et le phénobarbital ont été comparés à des rats contrôles recevant seulement le phénobarbital. L'altération de l'excrétion de l'eau dans la cirrhose expérimentale a été vérifiée par l'hyponatrémie basale (138 vs. 147 mEq/litre, P < 0,005) et le défaut d'excrétion d'une charge en eau (osmolalité urinaire minimale 262 vs. 100 mOsm/kg; 58 vs. 102% de la charge d'eau sont excrétés, P < 0,001). Pour élucider le mécanisme de cette altération de l'excrétion de l'eau le débit de filtration glomérulaire (GFR), le débit sanguin rénal (RBF) et les concentrations de vasopressine (VP) ont été mesurés. Dans la cirrhose GFR est normal alors que RBF est diminué (4,5 vs. 6,8 ml/min/gm, P < 0,01). VP est plus élevée chez les rats cirrhotiques (1,61 vs. 0,71 pg/ml, P < 0,025). La signification des modifications de l'hémodynamique rénale et de l'augmentation de VP a été évaluée en créant des cirrhoses chez des rats sans VP de la souche Brattleboro (DI). Malgré des modifications histologiques, biochimiques et hémodynamiques rénales qui sont comparables à celles des rats dont la neurohypophyse est intacte, les rats DI cirrhotiques n'ont pas d'altération de l'excrétion de l'eau. Pour connaître la cause de l'augmentation de VP dans la cirrhose expérimentale le volume sanguin et l'hémodynamique systémique ont été étudiés. Quoique le volume plasmatique soit augmenté dans la cirrhose expérimentale (4,3 vs. 3,0 ml/100 g, P < 0,05) les rats cirrhotiques ont des résistances périphériques inférieures (0,37 vs. 0,42mm Hg/ml/min/kg, P < 0,05) et une pression artérielle moyenne inférieure (104 vs. 120mm Hg, P < 0,001) à celles des rats contrôles. Ces résultats indiquent que la cirrhose expérimentale du rat comporte une altération de l'excrétion de l'eau associée à une hémodynamique rénale anormale et à des concentrations de VP augmentées. L'altération de l'excrétion de l'eau, cependant, a la vasopressione comme seul médiateur. Le stimulus non osmolaire de la libération de VP pourrait être l'anomalie de l'hémodynamique systémique

Phosphoinositide metabolism and prostacyclin formation in retinal microvascular endothelium: Stimulation by adenine nucleotides

Phosphoinositide lipid metabolism and prostacyclin production are implicated in endothelium dependent vascular relaxation in large blood vessels. To determine if these biochemical pathways might be involved in the regulation of microvascular tone in the retina, we measured the formation of 6-keto-prostaglandin-F1[alpha], the stable end product of prostacyclin, and inositol phosphates from 3H-labeled phosphoinositide lipids, in endothelial cells prepared from bovine retinal microvessels and maintained in long-term culture. We found that adenosine 5'-triphosphate and adenosine 5'-diphosphate both stimulated a dose-dependent accumulation of inositol phosphates and of 6-keto-prostaglandin-F1[alpha] in these cells. The agonist specificity of the responses, with stimulation by adenosine 5'-triphosphate and adenosine 5'-diphosphate, and inactivity of adenosine 5'-monophosphate and adenosine, suggest that they are mediated through P2 purinergic receptors. The similar early time courses of 6-keto-prostaglandin-F1[alpha] and inositol triphosphate production support the hypothesis that prostacyclin formation could result from the mobilization of intracellular calcium by inositol triphosphate, which activates phospholipase A, and thereby releases arachidonic acid to form prostacyclin. These findings point to a role for these cells in the regulation of normal retinal vascular tone. Because phosphoinositide lipid metabolism is altered in diabetes, dysfunction of these biochemical pathways in retinal endothelium could underlie the pathophysiology of diabetic retinopathy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28775/1/0000607.pd

Developing the framework for a risk map for mite vectored viruses in wheat resulting from pre-harvest hail damage

There is a strong economic incentive to reduce mite-vectored virus outbreaks. Most outbreaks in the central High Plains of the United States occur in the presence of volunteer wheat that emerges before harvest as a result of hail storms. This study provides a conceptual framework for developing a risk map for wheat diseases caused by mite-vectored viruses based on pre-harvest hail events. Traditional methods that use NDVI were found to be unsuitable due to low chlorophyll content in wheat at harvest. Site-level hyperspectral reflectance from mechanically hailed wheat showed increased canopy albedo. Therefore, any increase in NIR combined with large increases in red reflectance near harvest can be used to assign some level of risk. The regional model presented in this study utilized Landsat TM/ETMþ data and MODIS imagery to help gap-fill missing data. NOAA hail maps that estimate hail size were used to refine the area most likely at risk. The date range for each year was shifted to account for annual variations in crop phenology based on USDA Agriculture statistics for percent harvest of wheat. Between 2003 and 2013, there was a moderate trend (R2 ¼ 0.72) between the county-level insurance claims for Cheyenne County, Nebraska and the area determined to be at risk by the model (excluding the NOAA hail size product due to limited availability) when years with low hail claims (\u3c400 ha) were excluded. These results demonstrate the potential of an operational risk map for mite-vectored viruses due to pre-season hail events

Developing the framework for a risk map for mite vectored viruses in wheat resulting from pre-harvest hail damage

There is a strong economic incentive to reduce mite-vectored virus outbreaks. Most outbreaks in the central High Plains of the United States occur in the presence of volunteer wheat that emerges before harvest as a result of hail storms. This study provides a conceptual framework for developing a risk map for wheat diseases caused by mite-vectored viruses based on pre-harvest hail events. Traditional methods that use NDVI were found to be unsuitable due to low chlorophyll content in wheat at harvest. Site-level hyperspectral reflectance from mechanically hailed wheat showed increased canopy albedo. Therefore, any increase in NIR combined with large increases in red reflectance near harvest can be used to assign some level of risk. The regional model presented in this study utilized Landsat TM/ETMþ data and MODIS imagery to help gap-fill missing data. NOAA hail maps that estimate hail size were used to refine the area most likely at risk. The date range for each year was shifted to account for annual variations in crop phenology based on USDA Agriculture statistics for percent harvest of wheat. Between 2003 and 2013, there was a moderate trend (R2 ¼ 0.72) between the county-level insurance claims for Cheyenne County, Nebraska and the area determined to be at risk by the model (excluding the NOAA hail size product due to limited availability) when years with low hail claims (\u3c400 ha) were excluded. These results demonstrate the potential of an operational risk map for mite-vectored viruses due to pre-season hail events

Stress Preconditioning of Spreading Depression in the Locust CNS

Cortical spreading depression (CSD) is closely associated with important pathologies including stroke, seizures and migraine. The mechanisms underlying SD in its various forms are still incompletely understood. Here we describe SD-like events in an invertebrate model, the ventilatory central pattern generator (CPG) of locusts. Using K+ -sensitive microelectrodes, we measured extracellular K+ concentration ([K+]o) in the metathoracic neuropile of the CPG while monitoring CPG output electromyographically from muscle 161 in the second abdominal segment to investigate the role K+ in failure of neural circuit operation induced by various stressors. Failure of ventilation in response to different stressors (hyperthermia, anoxia, ATP depletion, Na+/K+ ATPase impairment, K+ injection) was associated with a disturbance of CNS ion homeostasis that shares the characteristics of CSD and SD-like events in vertebrates. Hyperthermic failure was preconditioned by prior heat shock (3 h, 45°C) and induced-thermotolerance was associated with an increase in the rate of clearance of extracellular K+ that was not linked to changes in ATP levels or total Na+/K+ ATPase activity. Our findings suggest that SD-like events in locusts are adaptive to terminate neural network operation and conserve energy during stress and that they can be preconditioned by experience. We propose that they share mechanisms with CSD in mammals suggesting a common evolutionary origin

The role of metrology in axSpA : does it provide unique information in assessing patients and predicting outcome? Results from the BSRBR-AS registry

ACKNOWLEDGMENTS We thank the staff who contributed to running the BSRBR-AS register and we also thank the recruiting staff at the clinical centers, details of which are available at: www.abdn.ac.uk/bsrbr-as.Peer reviewedPostprin

Angiogenesis in developing rat brain: An in vivo and in vitro study

Brain capillary proliferation in postnatal rats was measured in vivo by [3H]thymidine autoradiography. Maximal capillary proliferation occurred between 5 and 9 postnatal days, and was 40 times greater than in the adult. To test the hypothesis that soluble angiogenesis factors play a role in this developmental vascularization of brain, we prepared extracts from the brains of 6-day-old rats at the peak of proliferative activity, and from adults when it was lowest. We assayed them using an in vitro growth system measuring [3H]thymidine incorporation into cultured brain capillary endothelial cells. Extracts prepared from either 6-day or adult rats and containing 150 [mu]g/ml protein caused more than a 4-fold stimulation of the endothelial cells, increasing to 8-fold at a concentration of 1500 [mu]g/ml. The presence of growth-promoting activity in brain extracts from both adult and immature rats suggests that soluble angiogenesis factors may be present in the brain throughout life, but are unavailable for stimulation of in vivo capillary growth unless released or activated by an appropriate stimulus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25473/1/0000013.pd