scholarly journals Antidiuretic Action of a Corpus Cardiacum Factor (CTSH) on Long-Term Fluid Absorption Across Locust Recta in Vitro

1984 ◽  
Vol 113 (1) ◽  
pp. 409-421 ◽  
Author(s):  
B. PROUX ◽  
J. PROUX ◽  
J. E. PHILLIPS
Keyword(s):  
Active Transport ◽  
Chloride Transport ◽  
Rectal Wall ◽  
Fluid Absorption ◽  
Corpus Cardiacum ◽  
Osmotic Permeability ◽  
Antidiuretic Action ◽  
Stimulation Of

Long-term fluid absorption (Jv) by everted rectal sacs from locusts is stimulated by both corpus cardiacum (CC) extracts and cAMP in a dosedependent manner. This hormonal antidiuretic activity (ADH) is present in both nervous and glandular lobes of CC. This distribution is similar to that of chloride transport stimulating hormone (CTSH) but not to that of other factors previously reported from this gland. As expected if ADH were due to CTSH acting on electrogenic Cl− transport, CC extracts also increased the electropotential across rectal sacs, and the stimulation of fluid absorption ceased in Cl-free salines. CC extracts also caused recta to absorb fluid against larger osmotic gradients, suggesting that the antidiuretic factor acts on the ion-dependent active transport of fluid rather than on the osmotic permeability of the rectal wall.

Antidiuretic action of cyclic AMP, corpus cardiacum, and ventral ganglia on fluid absorption across locust ileum in vitro

1989 ◽  
Vol 67 (11) ◽  
pp. 2655-2661 ◽  
Author(s):  
R. A. Lechleitner ◽  
N. Audsley ◽  
J. E. Phillips
Keyword(s):  
Cyclic Amp ◽  
Fluid Transport ◽  
Physiological Saline ◽  
Dependent Manner ◽  
Fluid Absorption ◽  
Corpus Cardiacum ◽  
Ventral Ganglion ◽  
Osmotic Concentration ◽  
Osmotic Permeability

Locust ileal fluid transport (3.0–3.5 μL/h per ileum) and tissue volume were nearly constant after the 1st hour of incubation in physiological saline. Inhibition of absorption by KCN + iodoacetic acid and by azide indicated metabolic dependence of fluid transport. Fluid absorption occurred against osmotic concentration differences of up to 600 mosmol (luminal osmolarity > hemocoel osmolarity). Fluid absorption was stimulated by cyclic AMP, by both nervous and glandular lobes of the corpus cardiacum, and by the fifth ventral ganglion in a dose-dependent manner. All stimulants caused ilea to absorb against larger osmotic concentration differences. Stimulants in corpus cardiacum and fifth ventral ganglion extracts increased the osmotic permeability of the ileal wall at low osmotic concentration differences, whereas cyclic AMP had a much smaller effect on osmotic permeability. The absorbate remained hyperosmotic to the luminal saline under all conditions, and stimulants increased absorbate osmolarity.

Excretion in the house cricket: stimulation of rectal reabsorption by homogenates of the corpus cardiacum

1993 ◽  
Vol 185 (1) ◽  
pp. 305-323 ◽  
Author(s):  
J. H. Spring ◽  
S. A. Albarwani
Keyword(s):  
Time Course ◽  
Chloride Transport ◽  
Malpighian Tubule ◽  
Acheta Domesticus ◽  
Rectal Absorption ◽  
K Uptake ◽  
House Cricket ◽  
Tubule Fluid ◽  
Stimulation Of

1. We describe an in vitro perfused preparation of Acheta domesticus rectum which allows direct comparison of Malpighian tubule secretion and rectal absorption under identical conditions. Rectal absorption is stimulated four- to sixfold by corpora cardiaca (CC) homogenates and the stimulated rate is sufficiently rapid to account for all the fluid secreted by the tubules. 2. The time course for increased fluid absorption is similar to that required to stimulate electrogenic chloride transport in locusts and grasshoppers. Chloride is rapidly absorbed by the rectum under all conditions, along with lesser amounts of Na+ and K+. Unlike the situation in locusts, K+ uptake is unaffected by CC homogenates and the stimulated absorbate is NaCl-rich, similar in composition to the NaCl-rich tubule fluid produced under stimulated conditions. The absorbate is always slightly hypo-osmotic to the perfusate, reaching a maximum differential of approximately 15 mosmol l-1 following CC stimulation. 3. The antidiuretic factor that reduces tubule secretion does not promote fluid reabsorption by the rectum.

The nitric oxide synthase inhibitor, N-monomethyl-L-arginine blocks induction of a long-term potentiation-like phenomenon in rat medial frontal cortical neurons in vitro

1993 ◽  
Vol 70 (3) ◽  
pp. 1255-1259 ◽  
Author(s):  
A. V. Nowicky ◽  
L. J. Bindman
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Long Term Potentiation ◽  
Control Group ◽  
Term Potentiation ◽  
The Mean ◽  
Synthase Inhibitor ◽  
Stimulation Of

1. Nitric oxide has been implicated in the production of long-term depression (LTD) in the cerebellum and in the production of long-term potentiation (LTP) and LTD in the hippocampus. We now provide evidence of its involvement in the induction of long-term synaptic potentiation in in vitro slices in the cerebral cortex of the rat. 2. Intracellular recordings were made from layer V neurons in the medial frontal cortex, and excitatory synaptic potentials (EPSPs) were evoked by electrical stimulation of layers II/III. Tetanic stimulation of this pathway may induce LTD or LTP or no change at these synapses. First we established experimental conditions under which a long lasting potentiation could be induced with a high incidence (> 60%), namely perfusion of slices with 1 microM bicuculline methiodide, second the use of increased shock duration in the tetanic conditioning stimuli, third and most important the addition of QX-314 to the microelectrode to reduce potassium conductances. Because the potentiation of the mean EPSP slope was significantly greater than the control at 40-min postconditioning, but was declining throughout this period, we refer to it for brevity as LTP, but strictly class it as an LTP-like phenomenon. 3. The nitric oxide (NO) synthase inhibitor interfered with the production of LTP. In the control group of neurons (n = 13) the mean depolarizing slope of the EPSP at 30-min post-conditioning was 142.7 +/- 2% (mean +/- SE) of the prestimulation control.(ABSTRACT TRUNCATED AT 250 WORDS)

Voltage dependence and barium sensitivity of colonic K secretion in renal failure

1989 ◽  
Vol 256 (3) ◽  
pp. F490-F496 ◽  
Author(s):  
E. L. Siga ◽  
R. S. Martin ◽  
C. Ibarra ◽  
D. Veron ◽  
F. Ibarra ◽  
...  
Keyword(s):  
Renal Failure ◽  
Active Transport ◽  
Voltage Dependence ◽  
Apical Membrane ◽  
Distal Colon ◽  
K Channels ◽  
K Secretion ◽  
Stimulation Of

Net colonic K secretion (JKnet) is increased in rats and humans with chronic renal failure (CRF). To study whether transepithelial potential difference (PD), active transport forces and/or luminal K conductance play a role in this adaptation, experiments were performed in the colon of control, K-adapted, and CRF rats. Under basal conditions the PD in vivo in CRF was greater than in controls and not different from K-adapted rats. JKnet was comparable in vivo in CRF and K-adapted rats and was greater than in controls. Amiloride (10 microM) reduced PD and JKnet in K-adapted and CRF rats to levels comparable to controls. Under in vitro short-circuited conditions serosal-to-mucosal K flux (JKs----m) in distal colon was significantly increased in K-adapted and CRF animals compared with control, whereas barium caused a significant reduction in JKs----m in all groups of animals. The barium-sensitive component of K secretion was greater, however, in the two experimental groups (-0.2 +/- 0.02 and -0.2 +/- 0.07 in K-adapted and CRF animals, respectively, vs. -0.08 +/- 0.02 microeq.h-1.cm-2 in controls, P less than 0.05). However, luminal barium failed to completely inhibit the increase in K secretion observed in the experimental groups. These data suggest that an increase in PD that results in a rise in luminal negativity, stimulation of active transport, and an increase in barium-sensitive K channels and barium-insensitive pathways in apical membrane of distal colon participate in the mechanism by which net K secretion is increased in the large intestine of subjects with CRF.

Characterization of insulin glycation in insulin-secreting cells maintained in tissue culture

1997 ◽  
Vol 152 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Y H A Abdel-Wahab ◽  
F P M O'Harte ◽  
C R Barnett ◽  
P R Flatt
Keyword(s):  
Tissue Culture ◽  
Secretory Activity ◽  
Protein Glycation ◽  
Subsequent Exposure ◽  
Insulin Secreting Cells ◽  
Per Se ◽  
Stimulation Of

Abstract Characteristics of cellular insulin glycation were examined in the pancreatic B-cell line, BRIN-BD11. The extent of insulin glycation increased stepwise during 72 h of culture at 5·6–33·3 mmol/l glucose, attaining levels up to 27%. Glycation of insulin at 33·3 mmol/l glucose was rapid, reaching maximal values within 2 h, and not readily reversible during 2 to 24 h of subsequent exposure to 5·6 mmol/l glucose. Glycated insulin was readily secreted by BRIN-BD11 cells upon active stimulation with glucose and other secretagogues. Cellular insulin glycation was decreased by 66–80% by inhibitors of protein glycation, vitamin C, aminoguanidine or acetylsalicylic acid. Modulation of insulin-secretory activity of BRIN-BD11 cells by co-culture at high glucose with diazoxide, l-alanine or glibenclamide indicated that long-term stimulation of secretion was associated with a decrease in the extent of insulin glycation. Glycation of insulin in vitro was substantially less extensive than in BRIN-BD11 cells, although glucose-6-phosphate and glyceraldehyde-3-phosphate were 1·4- to 2·0-fold more reactive than glucose per se. These observations indicate that insulin is readily glycated and secreted from insulin-secreting cells under hyperglycaemic conditions in culture. Journal of Endocrinology (1997) 152, 59–67

Corpus cardiacum stimulated trehalose efflux from cockroach (Periplaneta americana) fat body: control by calcium

1985 ◽  
Vol 63 (1) ◽  
pp. 63-66 ◽  
Author(s):  
J. E. Steele ◽  
T. Paul
Keyword(s):  
Cyclic Amp ◽  
Periplaneta Americana ◽  
Saline Solution ◽  
Fat Body ◽  
Surrounding Medium ◽  
Physiological Saline ◽  
Corpus Cardiacum ◽  
Physiological Saline Solution ◽  
Stimulation Of

Cockroach fat body incubated in a simple physiological saline solution releases trehalose to the surrounding medium. The output of trehalose occurs in the absence of ambient Ca2+ and decreases slowly with time. In two separate experiments, 0.1 mM CaCl2 added to the saline increased the output of trehalose on average by 70% but higher concentrations of Ca2+ did not further increase the efflux of trehalose. Stimulation of trehalose efflux by corpus cardiacum extract is absolutely dependent on extracellular Ca2+, no increase occurring beyond the basal level in the absence of the ion. The activity of corpus cardiacum extract increases as the concentration of CaCl2 is increased to 0.5 mM. This concentration of Ca2+ in the saline permits the extract to increase trehalose efflux by as much as 60% above the basal level. Corpus cardiacum extract, as well as the hypertrehalocaemic agents cyclic AMP and theophylline, increase significantly the influx of Ca2+ into fat body in vitro. The basal efflux of trehalose from fat body and that stimulated by corpus cardiacum extract is not dependent on extracellular Mg2+.

The stimulation of sodium transport by aldosterone

1971 ◽  
Vol 262 (842) ◽  
pp. 323-332 ◽  
Keyword(s):  
Protein Synthesis ◽  
Active Transport ◽  
Sodium Transport ◽  
Apical Plasma Membrane ◽  
Transport Pathway ◽  
Receptor Sites ◽  
Rna And Protein Synthesis ◽  
Inhibitor Of Protein Synthesis ◽  
Stimulation Of

Aldosterone, the major sodium retaining hormone in man, will stimulate active transport of sodium across the urinary bladder of the toad, Bufo marinus in vitro , at physiological concentrations of the hormone.The in vitro action of aldosterone is mimicked by steroid hormones with known mineralocorticoid properties and it is competitively inhibited by other analogues, e.g. spironolactone and cortisone. Aldosterone is bound to physiological receptor sites within the transporting epithelial cells, chiefly within the nuclei, and is displaced from these binding sites specifically by structural analogues including other mineralocorticoids. Effects of aldosterone are dependent upon availability of metabolizable substrates to support the active transport of sodium. Although the stimulation of sodium transport by aldosterone can be specifically inhibited by actinomycin D, an inhibitor of RNA synthesis, and by puromycin, an inhibitor of protein synthesis, direct evidence of stimulation of new RNA and protein synthesis during the latent period with physiological concentrations of aldosterone is still lacking. It is possible, however, that the amounts of RNA and protein that are involved are too small to be detected by available techniques. Evidence is summarized which leads us to conclude that the increased sodium transport induced by aldosterone is the consequence of a reduced resistance of the apical plasma membrane of the transporting epithelia to the entry of sodium into the transport pathway.

scholarly journals The Molecular Mechanism of Chronic High-Dose Corticosterone-Induced Aggravation of Cognitive Impairment in APP/PS1 Transgenic Mice

2021 ◽  
Vol 13 ◽  
Author(s):  
Shen-Qing Zhang ◽  
Long-Long Cao ◽  
Yun-Yue Liang ◽  
Pu Wang
Keyword(s):  
Preclinical Model ◽  
High Dose ◽  
Term Administration ◽  
Amyloid Aβ ◽  
Β Amyloid ◽  
Stimulation Of ◽  
Bace 1

Clinical studies have found that some Alzheimer’s disease (AD) patients suffer from Cushing’s syndrome (CS). CS is caused by the long-term release of excess glucocorticoids (GCs) from the adrenal gland, which in turn, impair brain function and induce dementia. Thus, we investigated the mechanism of the effect of corticosterone (CORT) on the development and progression of AD in a preclinical model. Specifically, the plasma CORT levels of 9-month-old APP/PS1 Tg mice were abnormally increased, suggesting an association between GCs and AD. Long-term administration of CORT accelerated cognitive dysfunction by increasing the production and deposition of β-amyloid (Aβ). The mechanism of action of CORT treatment involved stimulation of the expression of BACE-1 and presenilin (PS) 1 in in vitro and in vivo. This observation was confirmed in mice with adrenalectomy (ADX), which had lower levels of GCs. Moreover, the glucocorticoid receptor (GR) mediated the effects of CORT on the stimulation of the expression of BACE-1 and PS1 via the PKA and CREB pathways in neuroblastoma N2a cells. In addition to these mechanisms, CORT can induce a cognitive decline in APP/PS1 Tg mice by inducing apoptosis and decreasing the differentiation of neurons.

Sign in / Sign up

Export Citation Format

Share Document