scholarly journals Mechanisms of zinc uptake in gills of freshwater rainbow trout: interplay with calcium transport

1996 ◽  
Vol 270 (5) ◽  
pp. R1141-R1147 ◽  
Author(s):  
C. Hogstrand ◽  
P. M. Verbost ◽  
S. E. Bonga ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Control Level ◽  
Inhibitory Effect ◽  
Chloride Cells ◽  
Water Addition ◽  
Uptake Mechanism ◽  
Basolateral Membranes ◽  
Control Value

The uptake mechanism of Zn2+ through the gill epithelium of freshwater rainbow trout was investigated both in intact animals and in isolated basolateral membranes. Involvement of the apical Ca2+ uptake sites in Zn2+ uptake was examined in vivo by pharmacological manipulation of the apical Ca2+ permeability. The apical entries of Ca2+ and Zn2+, but not Na2+ and Cl-, were inhibited by addition of La to the water. Addition of 1.0 microM La reduced the influxes of Ca2+ and Zn2+ to 22 +/- 3 and 53 +/- 7% (mean +/- SE) of the control value, respectively. Injection of CaCl2 also reduced the branchial influxes of Ca2+ and Zn2+. This treatment decreased the influx of Ca2- to 45 +/- 4% of the control level and the Zn2+ influx to 68 +/- 5%. These results strongly imply that Zn2+ passes across the apical membrane of the chloride cells of the gills via the same pathway as Ca2+. The presence of an active basolateral transporter for Zn2+ was investigated in vitro on isolated basolateral membranes. There was no ATP-dependent or Na2+(-)gradient driven transport of Zn2+ at physiological Zn2+ activities. The same system was used to study potential effects of Zn2+ on the basolateral Ca2+(-)adenosinetri-phosphatase. Zn2+ was found to be a potent blocker of this transporter, causing a mixed inhibitory effect on the ATP driven Ca2+ transport at a free Zn2+ activity of 100 pM.

scholarly journals Effects of potassium deficiency on growth and protein synthesis in skeletal muscle and the heart of rats

1989 ◽  
Vol 62 (2) ◽  
pp. 269-284 ◽  
Author(s):  
Inge Dôrup ◽  
Torben Clausen
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Protein ◽  
Control Level ◽  
Inhibitory Effect ◽  
Potassium Deficiency ◽  
Skeletal Muscle Protein ◽  
K Deficiency

The effects of potassium deficiency on growth, K content and protein synthesis have been compared in 4–13-week-old rats. When maintained on K-deficient fodder (1 mmol/kg) rats ceased to grow within a few days, and the incorporation of [3H]leucine into skeletal muscle protein in vivo was reduced by 28–38%. Pair-feeding experiments showed that this inhibition was not due to reduced energy intake. Following 14 d on K-deficient fodder, there was a further reduction (39–56 %) in the incorporation of [3H]leucine into skeletal muscle protein, whereas the incorporation into plasma, heart and liver proteins was not affected. The accumulation of the non-metabolized amino acid α-aminoisobutyric acid in the heart and skeletal muscles was not reduced. The inhibitory effect of K deficiency on 3H-labelling of muscle protein was seen following intraperitoneal (10–240 min) as well as intravenous (10 min) injection of [3H]leucine. In addition, the incorporation of [3H]phenylalanine into skeletal muscle protein was reduced in K-depleted animals. Following acute K repletion in vivo leading to complete normalization of muscle K content, the incorporation of [3H]leucine into muscle protein showed no increase within 2 h, but reached 76 and 104% of the control level within 24 and 72 h respectively. This was associated with a rapid initial weight gain, but normal body-weight was not reached until after 7 weeks of K repletion. Following 7 d on K-deficient fodder the inhibition of growth and protein synthesis was closely correlated with the K content of the fodder (1–40 mmol/kg) and significant already at modest reductions in muscle K content. In vitro experiments with soleus muscle showed a linear relationship between the incorporation of [3H]leucine into muscle protein and K content, but the sensitivity to cellular K deficiency induced in vitro was much less pronounced than that induced in vivo. Thus, in soleus and extensor digitorum longus (EDL) muscles prepared from K-deficient rats, the incorporation of [3H]leucine was reduced by 30 and 47 % respectively. This defect was completely restored by 24 h K repletion in vivo. It is concluded that in the intact organism protein synthesis and growth are very sensitive to dietary K deficiency and that this can only partly be accounted for by the reduction in cellular K content per se. The observations emphasize the need for adequate K supplies to ensure optimum utilization of food elements for protein synthesis and growth.

Paradoxical effect of perchlorate on thyroidal weight, glucose 6-phosphate dehydrogenase and polyamines in methylthiouracil-treated rats

1981 ◽  
Vol 97 (4) ◽  
pp. 491-495 ◽  
Author(s):  
S. Matsuzaki ◽  
M. Suzuki
Keyword(s):  
Enzyme Activity ◽  
Control Level ◽  
Sodium Perchlorate ◽  
Inhibitory Effect ◽  
Paradoxical Effect ◽  
G6pdh Activity ◽  
Wet Weight ◽  
Glucose 6 Phosphate Dehydrogenase

Abstract. The effect of sodium perchlorate (NaClO4) on the methylthiouracil-induced increase in the activity of thyroid glucose 6-phosphate dehydrogenase (G6PDH), ornithine decarboxylase (ODC) and polyamine contents was studied in the rat. The G6PDH activity was increased nearly three-fold by methylthiouracil (MTU) but not by ClO4- at 7 days of treatment. Perchlorate lowered the MTU-induced enzyme activity to nearly the control level, without changing circulating thyrotrophin (TSH). The anion had no inhibitory effect on G6PDH activity in vitro. The possibility that an inhibitor specific for G6PDH was generated in ClO4- treated rat thyroids was excluded. The activity of ODC was greatly increased by both ClO4- and MTU, the increase being significant as early as on the second day of treatment. Perchlorate had no inhibitory effect on MTU-induced ODC activity in vivo but decreased total contents of spermidine and spermine in the thyroid, without affecting the concentration (nmoles/ g wet weight) of the polyamines. These results suggest that ClO4- acts directly on the thyroid to suppress specifically the stimulatory effect of TSH on G6PDH activity and possibly on polyamine accumulation.

scholarly journals Calcium transport by isolated skin of rainbow trout

1992 ◽  
Vol 166 (1) ◽  
pp. 297-316 ◽  
Author(s):  
W. S. Marshall ◽  
S. E. Bryson ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Cell Density ◽  
Flux Ratio ◽  
Adenosine Monophosphate ◽  
Mucosal Surface ◽  
Chloride Cells ◽  
Serosal Surface ◽  
Ratio Criterion

The skin overlying the cleithrum bone of freshwater-acclimated rainbow trout contains numerous mitochondria-rich (MR) cells, as detected by DASPEI fluorescence. This tissue was mounted in vitro in an Ussing-style chamber with fresh water on the mucosal surface and saline supplemented with bovine serum albumin on the serosal surface. The preparation developed a high transepithelial resistance and a small transepithelial potential (Vt), positive on the serosal side. Radioisotopic flux measurements indicated that the preparation actively transported Ca2+ from the mucosal to the serosal surface, as assessed by the Ussing flux ratio criterion. Ca2+ transport was positively correlated with MR cell density. Cortisol pretreatment in vivo reduced MR cell density and increased Vt but did not significantly alter Ca2+ fluxes. Ca2+ transport was unaffected by adrenergic agonists (10(−5) mol l-1 adrenaline, clonidine, isoprenaline) or cyclic AMP stimulants (10(−3) mol l-1 dibutyryl cyclic adenosine monophosphate, db-cAMP, plus 10(−4) mol l-1 isobutylmethylxanthine, IBMX) applied to the serosal surface. The Ca2+ ionophore ionomycin (1 × 10(−6)-3.2 × 10(−6) mol l-1 on the mucosal surface) increased both unidirectional Ca2+ fluxes and caused Ca2+ to accumulate within the epithelium. Lanthanum (10(−4) mol l-1) did not inhibit unidirectional Ca2+ fluxes, but apparently displaced Ca2+ from binding sites on the mucosal surface. Unlike Ca2+, movements of Na+ and Cl- across the epithelium were passive, as assessed by the flux ratio criterion, and neither adrenaline nor db-cAMP plus IBMX had any effect on Na+ or Cl- fluxes or electrical properties. These results indicate that ion transport across the skin mediated by MR cells (‘chloride cells’) contributes to Ca2+ but not to NaCl balance in freshwater trout.

Interaction of glutamine and arginine on cerebrovascular reactivity to hypercapnia

2000 ◽  
Vol 278 (5) ◽  
pp. H1577-H1584 ◽  
Author(s):  
Toshiki Okada ◽  
Yukinaga Watanabe ◽  
Saul W. Brusilow ◽  
Richard J. Traystman ◽  
Raymond C. Koehler
Keyword(s):  
Ammonium Acetate ◽  
Inhibitory Effect ◽  
Cerebrovascular Reactivity ◽  
Control Group ◽  
Vascular Effect ◽  
Arginine Infusion ◽  
Control Value ◽  
Cranial Window

Glutamine is purported to inhibit recycling of citrulline to arginine and to limit nitric oxide release in vitro. However, vasoactive effects of glutamine have not been clearly demonstrated in vivo. During hyperammonemia, impaired cerebrovascular reactivity to CO2 is related to glutamine accumulation. We tested the hypotheses that 1) glutamine infusion in the absence of hyperammonemia impairs cerebrovascular CO2 reactivity and 2) arginine infusion preserves CO2 reactivity during glutamine infusion and during hyperammonemia. Pentobarbital sodium-anesthetized rats were equipped with a closed cranial window for measuring pial arteriolar diameter. Intravenous infusion of 3 mmol ⋅ kg− 1 ⋅ h− 1of l-glutamine for 6 h produced threefold increases in plasma and cerebrospinal fluid concentrations. Dilation to hypercapnia was reduced by 45% compared with that of a time control group at 6 h but not at 3 h of glutamine infusion. Coinfusion of 2 mmol ⋅ kg− 1 ⋅ h− 1of l-arginine with glutamine maintained the hypercapnic vasodilation at the control value. Infusion of ammonium acetate at a rate known to produce threefold increases in cortical tissue glutamine concentration resulted in no significant hypercapnic vasodilation. Coinfusion of arginine with ammonium acetate maintained hypercapnic vasodilation at 60% of the control value. Arginine infusion did not augment hypercapnic vasodilation in a control group. We conclude that glutamine modulates cerebrovascular CO2 reactivity in vivo. Glutamine probably acts by limiting arginine availability because the vascular inhibitory effect required >3 h to develop and because arginine infusion counteracted the vascular effect of both endogenously and exogenously produced increases in glutamine.

scholarly journals Kinetics of Branchial Calcium Uptake in the Rainbow Trout: Effects of Acclimation to Various External Calcium Levels

1985 ◽  
Vol 116 (1) ◽  
pp. 411-433 ◽  
Author(s):  
S. F. PERRY ◽  
C. M. WOOD
Keyword(s):  
Rainbow Trout ◽  
Calcium Uptake ◽  
Chloride Cells ◽  
Arterial Circulation ◽  
In Vivo Experiments ◽  
Kinetics Of ◽  
Fold Stimulation ◽  
External Calcium

Calcium uptake (JCain) in freshwater rainbow trout (Salmo gairdnen) under control conditions (external [Ca2+] ≃ 1.8 mequivl−1, [NaCl] ≃ 0.8 mequiv 1−1) occurred at approximately equal rates (12–15 μequiv kg−1 h−1) through the gills and the general body surface in vivo. The gut was not involved. Under the same conditions, in vitro branchial JCain in an isolated, saline-perfused head preparation was equal to that in vivo. The cells involved in JinCa are mainly located on lamellae rather than on filaments since 95 % of JinCa occurred across the arterio-arterial circulation of the gill. JinCa, in vitro, displayed Michaelis-Menten kinetics. Acclimation to low external [Ca2+] (50 μequiv 1−1; unchanged [NaCl]) for 1 day caused a five-fold stimulation of JinCa characterized by decreased Km and increased J max. Longer periods of low [Ca2+] acclimation resulted in changes of Jmax only. Jmax gradually returned towards control levels as acclimation time increased, but was still elevated after 30 days. Acclimation to low ambient [Ca2+] caused proliferation and increased exposure of lamellar chloride cells which were correlated with increased Jmax. Fish exposed to high external [Ca2+] (10 mequivl−1; unchanged [NaCl]) displayed reduced JinCa Similar changes in JinCa were observed during in vivo experiments. Plasma Ca2+ concentration remained constant regardless of external [Ca2+], while plasma Na+ and Cl− levels were transiently reduced at 1 day low [Ca2+] exposure but had recovered by 7 days. A possible role for cortisol in Ca2+ regulation is discussed based on observations of cortisol-stimulated lamellar chloride cell proliferation and JinCa, and elevated plasma [cortisol] in low-[Ca2+] acclimated fish.

Plasma Ultrafiltrable Calcium Concentration in Posthypercapnic Ventricular Fibrillation

1957 ◽  
Vol 190 (3) ◽  
pp. 462-466 ◽  
Author(s):  
E. B. Brown ◽  
Ananda S. Prasad
Keyword(s):  
Ventricular Fibrillation ◽  
Inorganic Phosphate ◽  
Control Level ◽  
Respiratory Acidosis ◽  
Sharp Decrease ◽  
Plasma Potassium ◽  
Total Calcium ◽  
Control Value

During four hours of severe respiratory acidosis produced by inhalation of 30% and 40% CO2 in dogs, plasma potassium and inorganic phosphate rose, ultrafiltrable calcium first increased then fell below control level, and total calcium increased slightly. Within 5 minutes after returning the animal to air breathing, potassium showed a further sharp increase, ultrafiltrable calcium a further sharp decrease and total calcium and inorganic phosphate showed no change. With the rise in potassium and fall in ultrafiltrable calcium the UF Ca/K ratio fell to less than one third control value. This appears to be an important factor in the mechanism producing cardiac arrhythmias and ventricular fibrillation in the immediate post-hypercapnic period. In vitro experiments on dog blood indicate that ultrafiltrable calcium varies directly with H+ concentration as expected, and that an increase in inorganic phosphate produces a decrease in ultrafiltrable calcium. Operation of these two factors helps to explain the change in plasma ultrafiltrable calcium observed in the in vivo experiments. It is suggested that the decrease in ultrafiltrable calcium in the presence of the very high phosphate concentrations observed, may be due to the formation of some nonfiltrable calcium phosphate compound. It is possible that the increased phosphate concentration increases the binding of calcium in some other form.

Comparison of Specific Antibody, D-Phe-Pro-Arg-CH2Cl and Aprotinin for Prevention of In Vitro Effects of Recombinant Tissue-Type Plasminogen Activator on Haemostasis Parameters

1987 ◽  
Vol 58 (03) ◽  
pp. 921-926 ◽  
Author(s):  
E Seifried ◽  
P Tanswell
Keyword(s):  
Specific Antibody ◽  
Plasma Concentrations ◽  
Fibrinolytic Therapy ◽  
Tissue Type ◽  
Control Value ◽  
Type Plasminogen Activator ◽  
In Vitro Effects ◽  
Fibrinolytic Parameters

SummaryIn vitro, concentration-dependent effects of rt-PA on a range of coagulation and fibrinolytic assays in thawed plasma samples were investigated. In absence of a fibrinolytic inhibitor, 2 μg rt-PA/ml blood (3.4 μg/ml plasma) caused prolongation of clotting time assays and decreases of plasminogen (to 44% of the control value), fibrinogen (to 27%), α2-antiplasmin (to 5%), FV (to 67%), FVIII (to 41%) and FXIII (to 16%).Of three inhibitors tested, a specific polyclonal anti-rt-PA antibody prevented interferences in all fibrinolytic and most clotting assays. D-Phe-Pro-Arg-CH2Cl (PPACK) enabled correct assays of fibrinogen and fibrinolytic parameters but interfered with coagulometric assays dependent on endogenous thrombin generation. Aprotinin was suitable only for a restricted range of both assay types.Most in vitro effects were observed only with rt-PA plasma concentrations in excess of therapeutic values. Nevertheless it is concluded that for clinical application, collection of blood samples on either specific antibody or PPACK is essential for a correct assessment of in vivo effects of rt-PA on the haemostatic system in patients undergoing fibrinolytic therapy.

The Effect of Barbituric Acid Derivatives on Platelet Function in Vitro and in Vivo

1973 ◽  
Vol 30 (02) ◽  
pp. 315-326
Author(s):  
J. Heinz Joist ◽  
Jean-Pierre Cazenave ◽  
J. Fraser Mustard
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Barbituric Acid ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Primary Response ◽  
Sodium Pentobarbital ◽  
Barbituric Acid Derivatives

SummarySodium pentobarbital (SPB) and three other barbituric acid derivatives were found to inhibit platelet function in vitro. SPB had no effect on the primary response to ADP of platelets in platelet-rich plasma (PRP) or washed platelets but inhibited secondary aggregation induced by ADP in human PRP. The drug inhibited both phases of aggregation induced by epinephrine. SPB suppressed aggregation and the release reaction induced by collagen or low concentrations of thrombin, and platelet adherence to collagen-coated glass tubes. The inhibition by SPB of platelet aggregation was readily reversible and isotopically labeled SPB did not become firmly bound to platelets. No inhibitory effect on platelet aggregation induced by ADP, collagen, or thrombin could be detected in PRP obtained from rabbits after induction of SPB-anesthesia.

Inhibition of Human and Animal Platelet Adhesiveness to Glass Bead Columns by Adenosine, Dipyridamole, Chlorpromazine and Acetylsalicylic Acid

1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu
Keyword(s):  
Guinea Pig ◽  
Acetylsalicylic Acid ◽  
Guinea Pigs ◽  
Glass Bead ◽  
Animal Species ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Platelet Adhesiveness

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.

Phenolic Acids Exert Anticholinesterase and Cognition-Improving Effects

2018 ◽  
Vol 15 (6) ◽  
pp. 531-543 ◽  
Author(s):  
Dominik Szwajgier ◽  
Ewa Baranowska-Wojcik ◽  
Kamila Borowiec
Keyword(s):  
Phenolic Acids ◽  
Ex Vivo ◽  
Amyloid Β ◽  
Inhibitory Effect ◽  
In Vivo Studies ◽  
Amyloid Β Peptide ◽  
Beneficial Effects ◽  
Aβ Fibrils

Numerous authors have provided evidence regarding the beneficial effects of phenolic acids and their derivatives against Alzheimer's disease (AD). In this review, the role of phenolic acids as inhibitors of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) is discussed, including the structure-activity relationship. In addition, the inhibitory effect of phenolic acids on the formation of amyloid β-peptide (Aβ) fibrils is presented. We also cover the in vitro, ex vivo, and in vivo studies concerning the prevention and treatment of the cognitive enhancement.

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