An Intelligent and Tumor-Responsive Fe2+ Donor and Fe2+-Dependent Drugs Cotransport System

2016 ◽  
Vol 8 (49) ◽  
pp. 33484-33498 ◽  
Author(s):  
Huijuan Zhang ◽  
Qianqian Chen ◽  
Xiaoge Zhang ◽  
Xing Zhu ◽  
Jianjiao Chen ◽  
...  
Keyword(s):  
Cotransport System

Use of Oral Fluid Therapy and Posttreatment Feeding Following Enteritis in Children in a Developed Country

PEDIATRICS ◽  
1985 ◽  
Vol 75 (2) ◽  
pp. 358-361
Author(s):  
Keyword(s):  
Developing Countries ◽  
Fluid Therapy ◽  
Oral Fluid ◽  
Electrolyte Solutions ◽  
Oral Hydration ◽  
Developed Country ◽  
Oral Rehydration ◽  
Young Infants ◽  
Life Threatening ◽  
Cotransport System

The 1982-1983 report by the United Nations Children's Fund (UNICEF) on the State of the World's Children recommended widespread implementation of oral rehydration as one of the four strategies projected to save the lives of 20,000 children each day.1 In the developing countries, oral rehydration has been shown to be an effective, simple, and inexpensive therapy for dehydration caused by severe enteritis in infants.2-8 The modern concepts of oral fluid therapy for diarrheal diseases evolved in part from the clinical observation that orally administered glucose-electrolyte solutions can replace diarrheal fluid losses in cholera. Previous laboratory investigation had demonstrated the presence of a cotransport system of sodium with glucose or other actively transported small organic molecules in the small intestine in animals and in man. Clinical studies suggest that this sodium-glucose cotransport system remains intact not only when the pathophysiologic agent is an enterotoxin, such as that elaborated by Vibrio cholerae or enterotoxigenic strains of Escherichia coli, but also with inflammatioion such as that associated with rotavirus, Campylobacter jejuni, E coli, and Yersinia enterocolitica.4-8 These observations have provided a physiologic rationale for an appropriately efficient ratio of sodium to glucose in formulating solutions to be used in the developing countries for oral therapy in the treatment of infants with life-threatening diarrheal dehydration. The question we address in this commentary is that of the appropriate implementation of oral hydration therapy in a developed country. Pediatricians and others concerned with the health of children in this country are not usually confronted with the problem of obtaining uncontaminated water nor with the management of large numbers of severely malnourished young infants with multiple health problems.

Effects of Synthetic Atrial Natriuretic Peptides on Sodium-Potassium Transport in Human Erythrocytes

1985 ◽  
Vol 69 (2) ◽  
pp. 223-226 ◽  
Author(s):  
G. A. Sagnella ◽  
D. A. Nolan ◽  
A. C. Shore ◽  
G. A. MacGregor
Keyword(s):  
Loop Diuretic ◽  
Sodium Pump ◽  
Human Erythrocytes ◽  
Atrial Natriuretic Peptides ◽  
Sodium Potassium ◽  
Potassium Ion Transport ◽  
Wide Range ◽  
Natriuretic Effect ◽  
Cotransport System ◽  
Sodium And Potassium

1. The effects of synthetic human and rat atrial peptides on sodium and potassium ion transport has been investigated in intact human erythrocytes. 2. The effects of these peptides have been tested on the active, sodium pump-dependent (ouabain-sensitive) and on the sodium-potassium cotransport system (bumetanide-sensitive) with 86Rb used as a tracer. 3. Human (α-ANP, 28 amino acids) or rat (atriopeptin III) atrial peptides, over a wide range of concentrations, did not influence the uptake of 86Rb in either the ouabain-sensitive or the bumetanide-sensitive transport system. 4. These results suggest that the natriuretic effect of the atrial peptides is not mediated through inhibition of the sodium pump or the loop-diuretic-sensitive Na-K cotransport.

Characterisation of the H(+)/peptide cotransporter of eel intestinal brush-border membranes

2000 ◽  
Vol 203 (19) ◽  
pp. 2991-3001 ◽  
Author(s):  
T. Verri ◽  
M. Maffia ◽  
A. Danieli ◽  
M. Herget ◽  
U. Wenzel ◽  
...  
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Anguilla Anguilla ◽  
Single Carrier ◽  
Catalytic Function ◽  
Negative Membrane Potential ◽  
Cotransport System ◽  
Polymerase Chain ◽  
Substrate Affinities

H(+)/peptide cotransport in brush-border membrane vesicles (BBMVs) from eel (Anguilla anguilla) intestine was studied by measuring d-[(3)H]-phenylalanyl-l-alanine uptake and by monitoring peptide-dependent intravesicular acidification using the pH-sensitive dye Acridine Orange. d-[(3)H]-phenylalanyl-l-alanine influx was greatly stimulated by an inside-negative membrane potential and enhanced by an inwardly directed H(+) gradient. In parallel, vesicular H(+) influx was significantly increased in the presence of extravesicular d-phenylalanyl-l-alanine or a series of glycyl and l-prolyl peptides. H(+)/peptide cotransport displayed saturable kinetics involving a single carrier system with apparent substrate affinities of 0.9-2.6 mmol l(−1) depending on the particular peptide. All substrates tested competed with this system. Pre-incubation of BBMVs with dipeptides prevented diethylpyrocarbonate inhibition of transport activity, suggesting that the substrates mask histidine residues involved in the catalytic function of the transporter. Using human PepT1-specific primers, a reverse transcription-polymerase chain reaction (RT-PCR) signal was detected in eel intestine. Our results suggest that, in eel intestine, a brush-border membrane ‘low-affinity’-type H(+)/peptide cotransport system is present that shares kinetic features with the mammalian intestinal PepT1-type transporters.

Acute Regulation of Na+:HCO3- Cotransport System In Kidney Proximal Tubules

1994 ◽  
pp. 309-317
Author(s):  
Manoocher Soleimani ◽  
Gwen L. Bizal ◽  
Yolanda J. Hattabaugh ◽  
Peter S. Aronson ◽  
Julia A. Bergman
Keyword(s):  
Proximal Tubules ◽  
Cotransport System ◽  
Kidney Proximal Tubules

Mechanisms of sodium and chloride transport across equine tracheal epithelium

1990 ◽  
Vol 259 (6) ◽  
pp. L459-L467 ◽  
Author(s):  
G. J. Tessier ◽  
T. R. Traynor ◽  
M. S. Kannan ◽  
S. M. O3'Grady
Keyword(s):  
Chloride Transport ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Short Circuit Current ◽  
Ringer Solution ◽  
Tracheal Epithelium ◽  
Ussing Chambers ◽  
Cl Secretion ◽  
Cotransport System ◽  
Ethanesulfonic Acid

Equine tracheal epithelium, stripped of serosal muscle, mounted in Ussing chambers, and bathed in plasmalike Ringer solution generates a serosa-positive transepithelial potential of 10–22 mV and a short-circuit current (Isc) of 70–200 microA/cm2. Mucosal amiloride (10 microM) causes a 40–60% decrease in Isc and inhibits the net transepithelial Na flux by 95%. Substitution of Cl with gluconate resulted in a 30% decrease in basal Isc. Bicarbonate substitution with 20 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid decreased the Isc by 21%. The Cl-dependent Isc was inhibited by serosal addition of 1 mM amiloride. Bicarbonate replacement or serosal amiloride (1 mM) inhibits the net Cl flux by 72 and 69%, respectively. Bicarbonate replacement significantly reduces the effects of serosal amiloride (1 mM) on Isc, indicating its effect is HCO3 dependent. Addition of 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP; 100 microM) causes a 40% increase in Isc. This effect is inhibited by subsequent addition of 10 microM serosal bumetanide. Bumetanide (10 microM) reduces net Cl secretion following stimulation with 8-BrcAMP (100 microM). Serosal addition of BaCl2 (1 mM) causes a reduction in Isc equal to that following Cl replacement in the presence or absence of 100 microM cAMP. These results suggest that 1) Na absorption depends on amiloride-inhibitable Na channels in the apical membrane, 2) Cl influx across the basolateral membrane occurs by both a Na-H/Cl-HCO3 parallel exchange mechanism under basal conditions and by a bumetanide-sensitive Na-(K?)-Cl cotransport system under cAMP-stimulated conditions, and 3) basal and cAMP-stimulated Cl secretion depends on Ba-sensitive K channels in the basolateral membrane.

Role of calcium in cAMP-mediated effects in the elasmobranch rectal gland

1983 ◽  
Vol 245 (6) ◽  
pp. R894-R900
Author(s):  
T. J. Shuttleworth
Keyword(s):  
Oxygen Consumption ◽  
Secretory Activity ◽  
Rectal Gland ◽  
Ouabain Binding ◽  
Calcium Dependent ◽  
Mediated Effects ◽  
Cotransport System ◽  
Vasodilatory Action ◽  
Potent Vasoconstrictor ◽  
Stimulation Of

The effects of A23187 and verapamil on the vasomotor and secretory effects of adenosine 3',5'-cyclic monophosphate (cAMP) in the rectal gland were investigated in Scyliorhinus canicula and Squalus acanthias. A23187 was a potent vasoconstrictor in the gland and reversed the vasodilatory action of cAMP in glands constricted with norepinephrine. Verapamil, like cAMP, prevented the vasoconstriction induced in the gland by norepinephrine. A23187 had no effect on the secretory activity (measured as ouabain binding and ouabain-sensitive oxygen consumption) of the glands. Verapamil inhibited the stimulation of ouabain binding, ouabain-sensitive oxygen consumption, and sodium secretion rate induced by cAMP plus theophylline, but did not affect the stimulation of ouabain binding and ouabain-sensitive oxygen consumption induced by amphotericin B. These data indicate that it is the cAMP-induced stimulation of the sodium-chloride cotransport system that is verapamil sensitive, and it is suggested that this stimulation is a calcium-dependent process. This emphasizes the independent nature of the secretory and vasomotor effects of the nucleotide in the gland.

Kinetic study of Na+-K+ pump in erythrocytes from essential hypertensive patients

1987 ◽  
Vol 252 (1) ◽  
pp. H1-H6 ◽  
Author(s):  
J. Diez ◽  
P. Hannaert ◽  
R. P. Garay
Keyword(s):  
Kinetic Study ◽  
Normal Limit ◽  
Maximal Rate ◽  
Normal Range ◽  
Apparent Dissociation Constant ◽  
Transport Pathways ◽  
Hypertensive Patients ◽  
L Cells ◽  
Na Efflux ◽  
Cotransport System

The interaction of the Na+-K+ pump with internal Na+ was investigated in erythrocytes from 38 normotensive control subjects and 49 essential hypertensive patients. In six of the hypertensive patients, the Na+-K+ pump exhibited an apparent dissociation constant for internal Na+ (KNa) above an upper normal limit of 7 mmol/l cells. Four of these six hypertensives showed an increase in the maximal rate of ouabain-sensitive Na+ efflux (Vmax), above an upper normal limit of 11 mmol X l cells-1 X h-1. These abnormalities were stable in repeated determinations over 1–3 yr. A kinetic study of other erythrocyte Na+ transport pathways showed that 16 hypertensives had a low apparent affinity of the Na+-K+ cotransport system for internal Na+, 10 hypertensives exhibited increased Na+-Li+ countertransport fluxes, and 11 hypertensives had increased Na+ leak. None of these three abnormalities were observed in the six hypertensives with abnormal pump fluxes. We thus propose to denominate them as Pump (-) hypertensives. Interestingly, four Pump (-) hypertensives exhibited an increased maximal rate of outward Na+-K+ cotransport. Basal erythrocyte Na+ content of Pump (-) hypertensives was within normal range. This suggests that the increased maximal rates of the Na+-K+ pump and Na+-K+ cotransport system compensate the low pump affinity for internal Na+.

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