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Biomedical subjects

C Amiel

Publications and source records attributed to C Amiel.

At least 109 records · Page 6Linked to original sources
PubMed1989

Effects of glucagon on Na+, Cl-, K+, Mg2+ and Ca2+ transports in cortical and medullary thick ascending limbs of mouse kidney.

The effects of glucagon on transepithelial Na+, Cl-, K+, Ca2+ and Mg2+ net fluxes were investigated in isolated perfused cortical (cTAL) and medullary (mTAL) thick ascending limbs of Henle's loop of the mouse nephron. Transepithelial ion net fluxes (JNa+, JCl-, JK+, JCa2+, JMg2+) were determined by electron probe analysis of the collected tubular fluid. Simultaneously the transepithelial voltage (PDte) and the transepithelial resistance (Rte) were recorded. In cTAL-segments (n = 8), glucagon (1.2 x 10(-8) mol.1-1) stimulated significantly the reabsorption of Na+, Cl-, Ca2+ and Mg2+: JNa+ increased from 204 +/- 20 to 228 +/- 23 pmol.min-1.mm-1, JCl- from 203 +/- 18 to 234 +/- 21 pmol.min-1.mm-1, JCa2+ from 0.52 +/- 0.13 to 1.34 +/- 0.30 pmol.min-1.mm-1 and JMg2+ from 0.51 +/- 0.08 to 0.84 +/- 0.08 pmol.min-1.mm-1.JK+ remained unchanged: 3.2 +/- 1.3 versus 4.0 +/- 1.9 pmol.min-1.mm-1. Neither PDte (16.3 +/- 1.5 versus 15.9 +/- 1.4 mV) nor Rte (22.5 +/- 3.0 versus 20.3 +/- 2.6 omega cm2) were changed significantly by glucagon. However, in the post-experimental periods a significant decrease in PDte and increase in Rte were noted. In mTAL-segments (n = 9), Mg2+ and Ca2+ transports were close to zero and glucagon elicited no significant effect. The reabsorptions of Na+ and Cl-, however, were strongly stimulated: JNa+ increased from 153 +/- 17 to 226 +/- 30 pmol.min-1.mm-1 and JCl- from 151 +/- 23 to 243 +/- 30 pmol.min-1.mm-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Renal functional reserve.

Renal functional reserve represents the capacity of the kidney to increase its level of operation in response to certain demands. The reserve of glomerular filtration rate and of renal blood flow is discussed from the following points of view: evaluation, measurement, mechanisms involved and significance. Data from the literature are discussed which show (i) that the mechanism of the hyperfiltration seen in the early stage of diabetic nephropathy may be different from the hyperfiltration induced by infusion of amino acids, (ii) that the remaining kidney in healthy kidney donors maintains its functional reserve, and (iii) that the functional reserve is fairly well maintained as long as the glomerular filtration rate is decreased only moderately. The reserve of tubular functional capacity is discussed from the point of view of concentration and dilution and of acidification and alkalinization.

Blood Flow Velocity↗
PubMed1989

Adaptation to Pi deprivation of cell Na-dependent Pi uptake: a widespread process.

Phosphate enters kidney proximal tubular cells through an apical sodium-phosphate cotransport; this activity (Vmax) increases during phosphate deprivation (Kidney Int. 18: 36-47, 1980). This study investigated the mechanism of phosphate uptake and its adaptation to phosphate deprivation in cultured cells from different origins (kidney, LLC-PK1 and MDCK cells; liver, Fao cells; heart, myocyte primary cultures). All cells exhibited a sodium-dependent phosphate uptake that was reduced (greater than 75%) by external sodium substitution and inhibited by ouabain (35%) and 2,4-dinitrophenol or KCN (80%). Phosphate deprivation (exposure to phosphate-free medium) increased sodium-dependent phosphate uptake by 1.8- to 5.8-fold and decreased cell inorganic phosphate and ATP contents (70-80 and 17-30%, respectively). The stimulation of phosphate uptake resulted from an increase in Vmax without change in Km and was dependent on gene transcription and protein synthesis because it was inhibited by cycloheximide and 3-deoxyadenosine. Thus a deprivation-stimulated, sodium-dependent phosphate transport was demonstrated in cells originating from distal kidney tubules, liver, and heart. The findings suggest that in hypophosphatemic diseases, impairment of renal proximal phosphate reabsorption might be only one expression of a widespread alteration of cell phosphate regulation.

Alanine↗
PubMed1989

Effects of lidocaine on sarcolemmal fluidity and cellular cAMP in rat cardiomyocytes.

Antiarrhythmic drugs with local anesthetic properties modify the physical state of membrane phospholipids and could change adenylate cyclase activity and, thus, influence cardiac ischemic arrhythmias. Adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cardiomyocytes cultured from newborn rat and fluorescence anisotropy of sarcolemma-enriched membranes were investigated in the presence of a neutral anesthetic drug benzyl alcohol and of a cationic anesthetic drug lidocaine. Benzyl alcohol increased in a dose-dependent manner both sarcolemma fluidity and isoproterenol- or cholera toxin-stimulated cAMP accumulation. In contrast, benzyl alcohol inhibited cAMP accumulation in forskolin-stimulated cells. Lidocaine induced a dose-related inhibition of isoproterenol-, forskolin-, and cholera toxin-stimulated cAMP accumulation without eliciting any change in sarcolemma fluidity. The inhibitory effect of lidocaine on isoproterenol-stimulated cAMP accumulation was reversed when cells were pretreated with pertussis toxin. These data suggest that the inhibitory effect of lidocaine on cAMP synthesis might involve a polar interaction with the Gi regulatory subunit of adenylate cyclase. Such an effect could contribute, in vivo, to both the antiarrhythmic and the negative inotropic effect of lidocaine.

Adenylate Cyclase Toxin↗
PubMed1989

Sodium transfer from endolymph through a luminal amiloride-sensitive channel.

An in vitro preparation of frog semicircular canal was devised to study the mechanisms of Na transport across the labyrinthine epithelium. When the lumen of the semicircular canal was filled with perilymph-like solution, the structure was able to secrete K into and to absorb Na from the lumen and to generate a lumen-positive transepithelial potential. When the lumen of the semicircular canal was filled with endolymph-like solution, the electrochemical composition of the luminal fluid was partly maintained up to 2 h. In this last experimental condition net and unidirectional fluxes were calculated in absence or presence of transport inhibitors, separately for the ampulla and for the nonampullar part of the canal. Amiloride (10(-5) M) but not dimethyl amiloride (10(-5) M) inhibited 60% of the unidirectional Na efflux out of endolymph; this Na efflux decrease resulted in an increase of the inward net Na flux. The net Na flux was also increased after abluminal application of ouabain (10(-3) M), furosemide (10(-4) M), and bumetanide (10(-6) M). This study validates this isolated preparation as a suitable tool for the study of endolymph secretion, confirms that the secretion of endolymph is achieved in the ampulla, and provides evidence for an apical amiloride-sensitive Na channel through which Na is transferred out of endolymph along an electrochemical gradient provided by the activity of the abluminal Na+-K+-ATPase.

Amiloride↗
PubMed1989

Decreased lymphocyte function-associated antigen-1 molecule expression on peripheral blood lymphocytes from patients with Graves' disease.

Humoral and cellular abnormalities have been described in autoimmune thyroid diseases, but a deficient cooperation between humoral and cellular systems has been poorly investigated in such diseases. Lymphocyte function-associated antigen-1 (LFA-1), a glycoprotein expressed on T- and B-lymphocytes, plays an important role in cell-cell interaction mechanisms and is involved in the homing phenomenon. The expression of this molecule was investigated on peripheral blood lymphocytes from patients suffering from various thyroid disorders. Decreased numbers of LFA-1-positive cells were observed in 30 patients with Graves' disease, while normal values were present in 8 patients with Hashimoto's thyroiditis and 37 subjects with nonautoimmune thyroid disorders. Treatment-induced improvement of Graves' disease was associated with an increase in LFA-1-positive cell number.

Adult↗
PubMed1988

Increase in membrane fluidity and opening of tight junctions have similar effects on sodium-coupled uptakes in renal epithelial cells.

Apical membranes of renal epithelial cells were shown to be more rigid than other plasma membranes, due in part to the abundance of sphingomyelin among their constituent phospholipids. Tight junctions play a key role in maintaining differences between the apical and the basolateral domains of the plasma membrane with respect to their lipid composition and fluidity. To evaluate the influence of alterations of membrane fluidity on the activity of two apically located transport systems, we compared the effect of opening of tight junctions, by a preincubation period in calcium-deprived medium and of increasing fluidity, with benzyl alcohol, on Na-dependent uptakes of Pi and alpha-methyl-D-glucopyranoside (MGP) in intact, confluent LLC-PK1 cells and MDCK cells. Benzyl alcohol, at 10 mM, increased the Vmax of Pi uptake by 55 and 42% in LLC-PK1 cells and MDCK cells, respectively, but decreased the Vmax of MGP uptake in LLC -PK1 cells by 23%. Similarly to 10 mM benzyl alcohol, opening of tight junctions also increased the Vmax of Pi uptake by 45 and 46% in LLC-PK1 cells and MDCK cells, respectively, and depressed MGP uptake in LLC-PK1 cells by inducing a 15% decrease of the Vmax. None of the two maneuvers (i.e. addition of benzyl alcohol or opening of tight junctions) affected the Km values of the transport systems. From these results it is concluded that (i) the increase in membrane fluidity, achieved either by benzyl alcohol or by opening of tight junctions, affects Na-Pi and Na-glucose cotransports differently, reflecting differences in the lipid environments of the two transport systems, and (ii) membrane fluidity might play a physiological role in the modulation of the activity of transport systems.

Animals↗
PubMed1988

Differential effects of ADH on sodium, chloride, potassium, calcium and magnesium transport in cortical and medullary thick ascending limbs of mouse nephron.

The effect of antidiuretic hormone (arginine vasopressin, AVP) on transepithelial Na+, Cl-, K+, Ca2+ and Mg2+ net transports was investigated in medullary (mTAL) and cortical (cTAL) segments of the thick ascending limb (TAL) of mouse nephron, perfused in vitro. Transepithelial net fluxes (JNa+, JCl-, JK+, JCa2+, JMg2+) were determined by electron probe analysis of the collected tubular fluid. Transepithelial potential difference (PDte) and transepithelial resistance (Rte) were measured simultaneously. cTAL segments were bathed and perfused with isoosmolal, HCO3- containing Ringer solutions, mTAL segments were bathed and perfused with isoosmolal HCO3- free Ringer solutions. In cTAL segments, AVP (10(-10) mol.l-1) significantly increased JMg2+ and JCa2+ from 0.39 +/- 0.08 to 0.58 +/- 0.10 and from 0.86 +/- 0.13 to 1.19 +/- 0.15 pmol.min-1 mm-1 respectively. Neither JNa+ nor JCl-, (JNa+: 213 +/- 30 versus 221 +/- 28 pmol.min-1 mm-1, JCl-: 206 +/- 30 versus 220 +/- 23 pmol.min-1 mm-1) nor PDte (13.4 +/- 1.3 mV versus 14.1 +/- 1.9 mV) or Rte (24.6 +/- 6.5 omega cm2 versus 22.6 +/- 6.4 omega cm2) were significantly changed by AVP. No significant effect of AVP on net K+ transport was observed. In mTAL segments, Mg2+ and Ca2+ net transports were close to zero and AVP (10(-10) mol.l-1) elicited no effect. However NaCl net reabsorption was significantly stimulated by the hormone, JNa+ increased from 107 +/- 33 to 148 +/- 30 and JCl- from 121 +/- 33 to 165 +/- 32 pmol.min-1 mm-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Tolerance of once-daily dosing of netilmicin and teicoplanin, alone or in combination, in healthy volunteers.

The purposes of this study were to test the pharmacokinetics and renal and otologic tolerances of a once-daily regimen of netilmicin and teicoplanin administered intramuscularly, alone or in combination (4.5 and 6 mg/kg, respectively), for 7 days in 30 healthy male volunteers. Teicoplanin induced only a mild increase in enzymuria. Nephrotoxicity was moderate and reversible with netilmicin; there was increased enzymuria and alteration in diluting ability, without significant changes in urinary beta 2-microglobulin levels, concentrating ability, and glomerular filtration rate. Ototoxicity was not detected in any of the subjects. Our results suggest that (1) teicoplanin and netilmicin given once daily induced only slight, reversible tubular damage, without any sign of ototoxicity; (2) their combination was not more toxic; and (3) clinical studies can be envisaged to evaluate the efficacy and tolerance of once-daily regimens in long-term treatment.

Acetylglucosaminidase↗
PubMed1988

Calcium and the inner ear fluids.

Total calcium (Ca) concentration in inner ear fluids was determined by fluorimetry, emission and absorption spectrophotometry, and electron probe analysis. The ionized Ca was measured with selective microelectrodes. In perilymph, the total Ca concentration (1.2 mM) was similar to the ultrafiltrable Ca concentration in plasma. The fraction of ionized Ca was 80%. In endolymph, a total Ca concentration of 0.5 mM contrasted with a reported ionized Ca concentration of 0.02 mM, which suggests, as a working hypothesis, that most of the Ca could exist as bicarbonate and/or phosphate undissociated salts. The decrease in the endocochlear potential induced an increase of the ionized fraction of the Ca. The electrochemical potential of Ca across the perilymph-endolymph barrier implies an active entry of Ca into the endolymph.

Calcium↗
PubMed1988

Possible role of Ca ions in the vestibular system.

The Ca++ messenger system is nearly universally present in the control of cell functions by extracellular messengers. It elicits different kinds of responses: either brief, as in neurotransmission and in skeletal muscle contraction, or sustained, as in smooth muscle contraction and in the regulation of transepithelial transport systems. In this latter function the Ca++ messenger system interacts with other cellular modulation systems such as cAMP production and arachidonic acid cascade. In the vestibular apparatus, the Ca++ messenger system is involved in the transduction processes in that it controls both the release of neurotransmitter at the basal pole of the hair cell and the electrical resonance of the cell. It also figures in the contractile properties of cochlear outer hair cells. The Ca++ messenger system as well as adenylate cyclase and prostaglandins may play an important role in the modulation of endolymph secretion.

Animals↗
PubMed1988

LFA1 expression in HIV infection.

The expression of the adhesion molecule LFA1 was investigated in mononuclear cells from 200 samples of peripheral blood obtained from asymptomatic HIV-infected individuals and AIDS patients. The numbers and percentages of LFAI-positive cells were established by indirect immunofluorescence. A significant decrease in the number of labelled cells was observed (mean percentage 68.9) while 100% of the cells were positive in controls. These data suggest that LFA1-mediated cell-cell cooperation might be impaired in HIV infection, adding to the immune deficiency related to the disappearance of CD4+ cells.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Benzyl alcohol increases membrane fluidity and modulates cyclic AMP synthesis in intact renal epithelial cells.

To evaluate a possible modulation by membrane fluidity of hormonal, cAMP-mediated effects on renal epithelial cells, we studied the effect of the neutral local anesthetic, benzyl alcohol, on membrane fluidity and on basal and stimulated intracellular cAMP content in intact MDCK cells. Benzyl alcohol induced a dose-dependent decrease of lipid order which was measured by steady-state fluorescence anisotropy using trimethylammonium-diphenylhexatriene and propionyl-diphenylhexatriene as fluorescent probes. Benzyl alcohol induced a 2-fold increase in basal cAMP content, likely as a consequence of increased prostaglandin synthesis since this effect was abolished by indomethacin. The effect of benzyl alcohol on stimulated cAMP synthesis depended on the nature of the ligand: 10 mM benzyl alcohol increased significantly the stimulatory effect of prostaglandin E2, glucagon and forskolin but not of vasopressin. At higher concentrations (40 mM), benzyl alcohol did not affect significantly the glucagon-stimulated cAMP content, while it inhibited significantly the prostaglandin E2-, forskolin- and vasopressin-stimulated cAMP synthesis. The 40 mM benzyl alcohol-induced inhibition was reversed by 1 mM Mn2+, which is known to block the inhibitory GTP-binding protein Ni. These results suggest that: (i) the various components of the adenylate cyclase-cAMP system and their coupling are affected differently by changes in membrane fluidity, which might reflect differences in their lipid environment, (ii) changes in membrane fluidity can modulate responses of renal tubular cells to hormones, and thus tubular functions.

Animals↗
PubMed1987

Protein kinase C activators and bradykinin selectively inhibit vasopressin-stimulated cAMP synthesis in MDCK cells.

To evaluate a possible modulation by protein kinase C of hormonal, cAMP-mediated effects on renal epithelial cells, we studied the effect of protein kinase C activators and of bradykinin on intracellular cAMP accumulation in MDCK cells. A 15-min pretreatment of cells with phorbol 12-myristate 13-acetate or 1-oleoyl-2-acetylglycerol induced a dose-dependent inhibition of vasopressin-stimulated cAMP synthesis, but not of basal or glucagon-, prostaglandin E2-, and forskolin-stimulated cAMP generation. 4 alpha-Phorbol 12,13-didecanoate, inactive on protein kinase C, did not affect cAMP accumulation. Bradykinin (0.1-10 microM) also inhibited the stimulatory effect of vasopressin on cAMP synthesis in a concentration-dependent manner, but affected neither basal cAMP content, nor its stimulation by glucagon, prostaglandin E2 and forskolin. The effect of activators of protein kinase C and of bradykinin occurred while renal prostaglandin synthesis was blocked with indomethacin. The inhibitory effect of protein kinase C activators and bradykinin on cAMP generation was reversed by the protein kinase C inhibitor H7, was enhanced by monensin, one effect of which is to block the recycling of membrane receptors, and persisted when the GTP-binding protein N1 was blocked with 1 mM Mn2+. Our data suggest that: protein kinase C can modulate the tubular effects of vasopressin by inhibiting cAMP generation; this effect is not mediated by renal prostaglandins, and might result from a direct action on the vasopressin receptor, or on its coupling with Ns; the modulation by bradykinin of vasopressin effects are likely to be exerted, at least partly, through activation of protein kinase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

Renal effects of platelet-activating factor in the rat.

The renal glomerular and tubular effects of the platelet-activating factor (Paf-acether) were studied, by clearance techniques, in acutely thyroparathyroidectomized Brattleboro rats infused with Paf-acether at the rate of 1.25, 2.5 or 5 ng/min/100 g bw. Paf-acether infusion was accompanied by decreases of urinary flow rate, calcium, and magnesium urinary excretion, whereas decreases of mean arterial pressure and glomerular filtration rate did not exceed 20% of control values for the highest perfusion rate of Paf-acether. These changes in tubular function were partially (calcium excretion) or totally (urinary flow rate and magnesium excretion) reversed after Paf-acether infusion was discontinued. Sodium and potassium excretion did not vary significantly during Paf-acether infusion, but increased dramatically after discontinuation of Paf-acether infusion. Infusion of lyso-Paf-acether or ethoxy-Paf-acether, two biologically less active structural analogues of Paf-acether, did not elicit any change in the variables studied. These data suggest that Paf-acether, when locally released by the kidney in pathological conditions, might affect both glomerular and tubular functions, possibly through different mechanisms.

Animals↗
PubMed1987

Vasopressin entry into the inner ear fluids of the rat.

The entry of arginine-vasopressin (AVP) and sucrose into cochlear endolymph, perilymph of scala vestibuli (PLV), perilymph of scala tympani (PLT), and cisternal cerebrospinal fluid (CSF) was studied, in anesthetized rats, after the administration into the cerebral lateral ventricle of a 10 microliter solution containing the radioactive tracers. Both tracers were detected in PLV, PLT, and CSF but not in endolymph. Monoexponential decay curves were calculated for PLV, PLT, and CSF, and for each tracer no difference was found between the regression lines calculated for the different fluids. These results indicate that (i) injection into the cerebral lateral ventricle is a useful tool to study the permeability of the cochlear epithelium to different solutes and (ii) no specific transport system exists for AVP across the cochlear epithelium, suggesting that AVP may exert its effect via the perilymphatic side of the stria vascularis.

Animals↗