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Biomedical subjects

C Amiel

Publications and source records attributed to C Amiel.

At least 91 records · Page 5Linked to original sources
PubMed1991

Antidiuretic hormone stimulation of adenylate cyclase in semicircular canal epithelium.

Basal adenosine 3',5'-cyclic monophosphate (cAMP) content and the modulation of its production were studied in the frog's semicircular canal epithelium. This epithelium secretes endolymph, a K(+)-rich, positively polarized fluid. The basal cAMP content measured by microradioimmunoassay was 244 +/- 14.2 fmol/structure per 5 min (n = 30). This content was increased about 8 times by 10(-5) M forskolin. Vasotocin, the frog antidiuretic hormone, increased the cAMP production by factors of 1.3 and 3.3 at concentrations of 10(-8) M and 10(-7) M, respectively. This stimulatory effect of vasotocin was blunted by the addition of alpha 2-adrenergic agonists, such as 10(-8) M-10(-5) M norepinephrine, in the presence of 10(-5) M propranolol, or 10(-5) M clonidine. Prostaglandin E2 at a concentration of 10(-8) M, which did not affect the cAMP production, did not modify the response to vasotocin. Glucagon (10(-6) M), calcitonin (10(-6) M), and parathyroid hormone (10 units/ml) did not affect the cAMP content. Prostaglandin E2 (10(-7) M) and the beta-adrenergic agonist isoproterenol (10(-6) M) stimulated the cAMP production by a factor of 1.6. These results indicate that the frog semicircular canal is a target of both vasotocin and catecholamines and that catecholamines through alpha 2-receptors modulate vasotocin-induced cAMP generation. Further, this interaction might be of physiological relevance in the modulation of ion transport in this structure.

Adenylyl Cyclases↗
PubMed1991

PKC and Pi deprivation modulate differently the ubiquitous Na-dependent Pi uptake in MDCK cells.

The role of protein kinase C (PKC) in the modulation of the ubiquitous sodium-dependent phosphate transport and in adaptation of that transport to phosphate deprivation was investigated in MDCK cells. Phorbol myristate acetate (PMA) had a biphasic effect on sodium-dependent phosphate uptake characterized by early inhibition (-25% at 1 h) followed by late stimulation (2.3-fold at 15 h). Late stimulation was related to a decreased apparent affinity (Km) with unchanged maximal velocity (Vmax). The 15-h stimulation of phosphate uptake was also induced by an initial 1-h PMA treatment followed by a 14-h washout of PMA or by R59 022. The stimulation was inhibited by PKC downregulation. PMA stimulation was dependent on protein synthesis but not on transcription, as shown by the respective effects of cycloheximide, 3'-deoxyadenosine, and actinomycin D. In phosphate-deprived cells PMA had also a biphasic effect. A potentiation of PMA stimulation of phosphate uptake with phosphate deprivation was observed. Adaptation to phosphate deprivation was not prevented by PKC downregulation. Cytosolic and membranous PKC activities were not changed by 15-h phosphate deprivation. We conclude that 1) PKC modulates sodium-dependent phosphate uptake in MDCK cells, and 2) phosphate deprivation and PKC modulation of sodium-dependent phosphate uptake involve different cellular pathways; that is, phosphate deprivation acts through gene regulation, and PKC acts through translation regulation.

Adaptation, Physiological↗
PubMed1991

Protein kinase C modulates cAMP content in proximal tubular cells: role of phosphodiesterase inhibition.

The present study was designed to evaluate whether protein kinase C (PKC) activation affects hormone-modulated adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in rabbit renal proximal tubular cells in primary culture. When intracellular cAMP content was measured in the presence of Ro 20-1724, a selective inhibitor of type III phosphodiesterase (PDE), activation of PKC by the phorbol ester phorbol 12-myristate 13-acetate (PMA) or by diacylglycerol kinase inhibitor R 59022 reinforced parathyroid hormone (PTH)- and forskolin-stimulated cAMP accumulation. During PKC activation, the inhibitory effect of norepinephrine on cAMP content persisted, whereas that of angiotensin II (ANG II) was blunted. In contrast, PKC activators had no effect on cAMP content during PDE blockade by the nonspecific inhibitor 3-isobutyl-1-methylxanthine (IBMX). These data suggested that PKC might affect cAMP degradation through inactivation of a Ro 20-1724-insensitive PDE. The possibility that the involved PDE was calcium sensitive was assessed; during PDE inhibition by Ro 20-1724, but not by IBMX, calcium ionophore A23187 inhibited PTH-stimulated cAMP accumulation and PMA abolished the effect of A23187. Finally, neither PKC inhibition by staurosporine nor its downregulation modified the magnitude of PTH-induced cAMP accumulation. In conclusion, 1) in proximal tubular cells PKC affects cAMP degradation rather than synthesis, possibly via inactivation of a calcium-sensitive PDE; 2) PKC modulates PTH-ANG II interaction; and 3) this pathway is likely to play a role in the fine tuning of the effect of PTH and ANG II in the proximal tubule.

Angiotensin II↗
PubMed1991

[Culture of the epithelium of middle ear in the study of seromucous otitis].

Preliminary results on transport properties of middle ear epithelium in primary culture are reported. Primary cultures of Mongolian gerbil (Meriones unguiculatus) middle ear epithelial cells were undergone. These cells formed polarized monolayers that exhibited domes when grown to confluence on non porous support. Domes are the consequence of active transepithelial transports of solutes and water. On porous support, Na+ and Cl- accumulated in the basal bath and generated a basolateral hyperosmolarity that drove a net water flow. This solutes and water absorption was the consequence of an active Na+ transcellular transport, by means of apical sodium channels, that was responsible for the transepithelial potential difference, lumen negative: -39 +/- 1.2 mV (mean +/- SEM, n = 63). Transport of fluid and ions in the middle ear cavities could play a major role in keeping the cavities fluid-free and air-filled and modulating the mucociliary clearance. Modulation of these transports could be involved at the start of otitis media with effusion, and would contribute to the mucociliary clearance impairment.

Absorption↗
PubMed1991

[The functional renal reserve].

The term "renal functional reserve" (RFR) refers commonly to the reserve of glomerular filtration rate (GFR) and renal blood flow. RFR can be elicited by an oral protein load or by infusion of amino acids, glucagon, or dopamine. The increase in GFR which follows amino acid administration results from a cascade of events including pancreatic release of glucagon, involvement of an hepatic step, and renal synthesis of vasodilatory prostaglandins. RFR represents a constant fraction of baseline GFR as long as the latter is above 40-50 ml/min. RFR becomes virtual for lower values of GFR. It has been suggested that permanent challenge of RFR, which occurs in protein-rich diet or during the hyperfiltration phase of diabetic nephropathy, might lead to and accelerate impairment of renal function. The relevance of RFR measurement as a tool to predict the evolution of renal function in various types of renal diseases remains to be evaluated.

Amino Acids↗
PubMed1990

CD4-like molecules in human sperm.

The expression of a molecule recognized by CD4 monoclonal antibodies was investigated on human sperm using immunolabelling, biochemical and immunochemical methods. Flow cytometry detected a significant fluorescence signal. SDS-PAGE analysis and Western blotting identified a molecule of 60 kDa, consistent with a CD4-like structure as confirmed after selective immunoseparation. Additional bands reacting with anti-CD4 were found in sperm extracts (73 kDa) and seminal fluid (90 kDa). These data indicate that sperm express a molecule similar to the receptor for HIV described on mononuclear cells.

Antigens, CD↗
PubMed1990

Increase in membrane fluidity modulates sodium-coupled uptakes and cyclic AMP synthesis by renal proximal tubular cells in primary culture.

In order to evaluate the influence of membrane fluidization on three apical transport systems and on a basolateral enzyme, and to analyse the mechanisms involved, we studied, in cultured rabbit proximal tubular cells, the effect of increasing concentrations of the local anesthetic drug benzyl alcohol on Na(+)-dependent uptakes of phosphate (Pi), methyl alpha-D-glucopyranoside (MGP), and L-alanine, as well as on basal and stimulated cyclic AMP content. At 10 mM, benzyl alcohol increased the Vmax of Pi uptake by 31%, decreased that of MGP uptake by 24%, and did not affect alanine uptake. Km values were not affected. Benzyl alcohol, up to 40 mM, increased in a concentration-dependent manner basal, PTH-stimulated, and cholera toxin-stimulated, but not forskolin-stimulated cyclic AMP accumulation. In the presence of 40 mM benzyl alcohol, the magnitude of PTH-induced inhibition of Pi uptake was enhanced from 11% to 24%. It is concluded that: (i) fluidization of apical membranes affected differently Na+/Pi, Na+/MGP, and Na+/alanine cotransports, reflecting differences in the lipidic environments of these transport system; (ii) fluidization of basolateral membranes enhanced PTH-stimulated cyclic AMP generation through improved coupling between the receptor-GS complex and the catalytic subunit of adenylate cyclase; (iii) these variations may result in physiological and pathophysiological modulation of the renal handling of solutes and of the phosphaturic effect of PTH.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Effects of parathyroid hormone and calcitonin on Na+, Cl-, K+, Mg2+ and Ca2+ transport in cortical and medullary thick ascending limbs of mouse kidney.

The effect of parathyroid hormone (PTH) on transepithelial Na+, Cl-, K+, Ca2+ and Mg2+ transport was investigated in isolated perfused cortical thick ascending limbs (cTAL) and that of human calcitonin (hCT) was tested in both cortical and medullary thick ascending limbs (mTAL) of the mouse nephron. The transepithelial ion net fluxes (Jx) were determined by electron probe analysis of the perfused and collected fluids. Simultaneously, the transepithelial voltage (PDte) and resistance (Rte) were recorded. In cTAL segments, PTH and hCT significantly stimulated the reabsorption of Na+, Cl-, Ca2+ and Mg2+, hCT generated a net K+ secretion towards the lumen and PTH tended to exert the same effect. Neither PDte nor Rte were significantly altered by either PTH or hCT. However, in the post-experimental period a significant decrease in PDte was noted. Time control experiments carried out under similar conditions revealed a significant decrease in PDte with time, which could have masked the hormonal response. In mTAL segments, Mg2+ and Ca2+ transport was close to zero, hCT did not exert any detectable effect on either PDte or Jcl-, JNa+, JK+, JMg2+ and JCa2+ in these segments. In conclusion, our data demonstrate that PTH and hCT stimulate NaCl reabsorption as well as Mg2+ and Ca2+ reabsorption in the cTAL segment of the mouse. These data are in agreement with and extend data obtained in vivo in the rat.

Animals↗
PubMed1990

Glucagon secretion is essential for aminoacid-induced hyperfiltration in man.

The role of glucagon as a mediator of aminoacid-induced alteration of renal haemodynamics was evaluated in man in three different protocols. In the first it was shown that the increase in glomerular filtration rate (GFR) and renal plasma flow (RPF) observed during an aminoacid infusion was prevented by the additional infusion of somatostatin (SRIF), but reproduced by a glucagon infusion in the presence of SRIF. In the second protocol it was shown that, at variance with normal subjects, six totally pancreatectomised patients, thus deprived of pancreatic glucagon secretion, did not increase their GFR and RPF when infused with amino-acids, whereas they exhibited the expected hyperfiltration when infused with glucagon. In the third protocol it was shown that glucagon infusion in a renal artery did not alter the homolateral renal haemodynamics. It is concluded that glucagon secretion is a mandatory step in the cascade of events linking the infusion of aminoacids to the renal hyperfiltration. Other steps beyond glucagon secretion are necessarily involved because glucagon has no direct renal effect.

Adult↗
PubMed1990

Isoproterenol increases Ca, Mg, and NaCl reabsorption in mouse thick ascending limb.

The effect of isoproterenol (Iso) on tubular transport in the thick ascending limb of Henle's loop (TAL) was investigated by in vitro microperfusion of MTAL (medullary) and CTAL (cortical) from White Swiss mouse kidney. The pattern of activation of adenylate cyclase along the distal tubule was investigated in this strain: results indicated that Iso stimulated adenylate cyclase fivefold in MTAL and ninefold in CTAL. Data from microperfusion experiments showed that Iso (10(-7) M in the bath) significantly and reversibly increased Ca and Mg reabsorption in CTAL. No net transport of Ca and Mg was observed in MTAL whether Iso was present or not. With regard to Na and Cl, Iso significantly stimulated their reabsorption in both segments and increased the transepithelial voltage in MTAL. Iso abolished K reabsorption in MTAL and induced a net K secretion in CTAL, the latter effect being also observed with 10(-9) M of Iso. When applied on CTAL, propranolol (10(-6) M in the bath) inhibited all these effects. These data indicate that beta-adrenergic agonists are involved in the multihormonal modulation of the TAL function.

Absorption↗
PubMed1990

12-HETE modulates Na-coupled uptakes in proximal tubular cells: role of diacylglycerol kinase inhibition.

Inhibition of diacylglycerol (DAG) kinase, an alternative way to increase the cellular DAG level, was shown to reproduce, in renal proximal tubular cells, the inhibitory effect of protein kinase C (PKC) activators on Na-Pi and Na-alpha-methyl-D-glucopyranoside (MGP) cotransport. To evaluate whether 12S-hydroxyeicosatetraenoic acid (12S-HETE) or 12R-HETE, a DAG kinase inhibitor in endothelial cells, has a similar effect in proximal tubular cells, we studied the influence of this lipoxygenase product on Na-dependent uptake of Pi, MGP, and alanine, as well as on [14C]arachidonate-DAG content and [32P]phosphatidic acid (PA) content in rabbit proximal tubular cells grown as a primary culture. 12-HETE (1-10 microM) decreased [32P]PA content and stimulated [14C]DAG accumulation in a concentration-dependent manner. The labeled phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin contents were not modified. 12-HETE also decreased DAG kinase activity of cell membranes. 12-HETE (10 microM) decreased the maximum velocity of Pi uptake by 36% and that of MGP uptake by 44% but did not affect alanine uptake. The effect of 12-HETE on transport was potentiated by calcium ionophore A23187 and was blunted by PKC downregulation. The effects of 12-HETE on lipid composition and transport were mimicked by R 59022, a pharmacological DAG kinase inhibitor. Neither arachidonic acid nor prostaglandin E2 reproduced the effects of 12-HETE. We conclude that in the proximal tubule, 12-HETE affected Na-dependent Pi and MGP cotransport through stimulation of PKC and that 12-HETE-induced activation of PKC is mediated by the inhibition of DAG kinase.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1990

[Hyponatremia in the aged person].

Hyponatremia occurs frequently in the elderly. During aging, mechanisms which regulate the renal handling of water are modified, making easier the occurrence of hyponatremia: osmotic and non osmotic release of ADH is increased whereas renal diluting capacity is depressed. Hyponatremia occurs predominantly during administration of diuretic therapy and/or in congestive cardiac failure. In those circumstances, hyponatremia results from increased non osmotic release of ADH, changes in renal hemodynamics and excessive water intake, as compared to renal diluting capacity. Intracellular hyperhydratation may lead to neurologic damage resulting either from the disorder itself or from a too rapid correction. The latter may be complicated by a cerebral demyelination syndrome. This risk makes necessary to define rules for correction of hyponatremia.

Aged↗
PubMed1989

Protein kinase C activation has dissimilar effects on sodium-coupled uptakes in renal proximal tubular cells in primary culture.

Protein kinase C (Ca2+/phospholipid-dependent enzyme) was shown to be present in renal brush border membranes. To evaluate the influence of protein kinase C activation on three apical transport systems, we studied the effect of phorbol myristate acetate (PMA) and of two diacylglycerol analogs, oleoylacetylglycerol and dioctanoylglycerol, on sodium-dependent uptakes of phosphate (Pi), L-alanine, and alpha-methyl-D-glucopyranoside (MGP), as well as on specific phlorizin binding, in cultured rabbit proximal tubular cells. PMA, at 100 ng/ml, decreased the Vmax of Pi and MGP uptake by 30 and 17%, respectively, but not that of alanine uptake. None of the Km values were affected. PMA also decreased the number of phlorizin binding sites by 40%. PMA-induced inhibition of Pi and MGP uptake was time- and concentration-dependent, was mimicked by oleoylacetylglycerol, dioctanoylglycerol, and the diacylglycerol kinase inhibitor R59022, and was reversed by the protein kinase C antagonist 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7). The effects of PMA persisted in the presence of amiloride and dimethyl amiloride, and were potentiated by Ca2+ ionophore A23187. Opening of tight junctions blunted subsequent PMA-induced decrease of MGP uptake, but not of Pi uptake. It is concluded that: (i) activation of protein kinase C does not affect similarly Na-Pi, Na-hexose, and Na-alanine cotransport; and (ii) different pathways are likely to be involved in the observed effects.

Amino Acids↗