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Biomedical subjects

P Bouyer

Publications and source records attributed to P Bouyer.

8 recordsLinked to original sources
PubMed2001

Atom laser divergence.

We measure the angular divergence of a quasicontinuous, rf-outcoupled, free-falling atom laser as a function of the outcoupling frequency. The data are compared to a Gaussian-beam model of laser propagation that generalizes the standard formalism of photonic lasers. Our treatment includes diffraction, magnetic lensing, and interaction between the atom laser and the condensate. We find that the dominant source of divergence is the condensate-laser interaction.

Journal Article↗
PubMed2001

Quasicontinuous atom laser in the presence of gravity.

We analyze the extraction from a trapped Bose-Einstein condensate to a nontrapping state of a coherent atomic beam and its subsequent fall, at T = 0 K. Our treatment fully takes gravity into account but neglects the mean-field potential exerted on the free falling beam by the trapped atoms. We derive analytical expressions for the output rate and the output mode of the quasicontinuous "atom laser." Comparison with experimental data of Bloch et al. [Phys. Rev. Lett. 82, 3008 (1999)] is satisfactory.

Journal Article↗
PubMed1999

Ammonium transport by the colonic H(+)-K(+)-ATPase expressed in Xenopus oocytes.

Functional expression of the rat colonic H(+)-K(+)-ATPase was obtained by coexpressing its catalytic alpha-subunit and the beta(1)-subunit of the Na(+)-K(+)-ATPase in Xenopus laevis oocytes. We observed that, in oocytes expressing the rat colonic H(+)-K(+)-ATPase but not in control oocytes (expressing beta(1) alone), NH(4)Cl induced a decrease in (86)Rb uptake and the initial rate of intracellular acidification induced by extracellular NH(4)Cl was enhanced, consistent with NH(+)(4) influx via the colonic H(+)-K(+)-ATPase. In the absence of extracellular K(+), only oocytes expressing the colonic H(+)-K(+)-ATPase were able to acidify an extracellular medium supplemented with NH(4)Cl. In the absence of extracellular K(+) and in the presence of extracellular NH(+)(4), intracellular Na(+) activity in oocytes expressing the colonic H(+)-K(+)-ATPase was lower than that in control oocytes. A kinetic analysis of (86)Rb uptake suggests that NH(+)(4) acts as a competitive inhibitor of the pump. Taken together, these results are consistent with NH(+)(4) competition for K(+) on the external site of the colonic H(+)-K(+)-ATPase and with NH(+)(4) transport mediated by this pump.

Animals↗
PubMed1998

Extracellular ATP raises cytosolic calcium and activates basolateral chloride conductance in Necturus proximal tubule.

1. Extracellular nucleotides modulate ionic transport mechanisms in various epithelia. In the present study, we investigated the effects of extracellular ATP on the intracellular free Ca+2 concentration ([Ca2+]i) and electrophysiological properties of Necturus maculosus proximal convoluted tubule (PCT). 2. ATP raised [Ca2+]i in microdissected fura-2-loaded PCTs (half-maximal effect, approximately mumol 1(-1) ATP). The initial ATP-induced changes in [Ca2+]i were not blunted by the removal of external Ca2+ nor by the presence of Ca2+ channel blockers, but were abolished by thapsigargin and suramin. The sequence for the potency of various agonists on [Ca2+]i was 2-methylthioATP (2MeSATP) = ADP = ATP >> UTP, 2',3',-O-(4-benzoilbenzoil) ATP (BzATP), alpha, beta-methylene ATP (AMPCPP), adenosine. 3. In vivo electrophysiological measurements showed that 100 mumol 1(-1) peritubular ATP added to a Ringer solution reduced the basolateral cell membrane potential (Vm) and increased the cell membrane input conductance. In a low Cl- solution, this ATP-induced depolarization was enhanced. These effects were inhibited by 1 mmol l-1 SITS, consistent with the activation of a basolateral Cl- conductance. 4. The ATP-induced change in Vm was reproduced by ADP but not by UTP or adenosine, and was prevented by suramin. 5. The ATP-induced membrane depolarization was not influenced by thapsigargin, BAPTA AM, or staurosporine and was not reproduced by manoeuvres increasing [Ca2+]i or intracellular cAMP content. 6. We conclude that, in Necturus PCT, a P2y receptor mobilizes Ca2+ mainly from intracellular pools and increases a basolateral Cl- conductance, GCl. The activation of GCl occurs by a mechanism which is not related either to an increase in [Ca2+]i or cAMP content, or to PKC activation.

Adenosine Triphosphate↗
PubMed1998

Does the colonic H,K-ATPase also act as an Na,K-ATPase?

We previously have demonstrated that the colonic P-ATPase alpha subunit cDNA encodes an H,K-ATPase when expressed in Xenopus laevis oocytes. Besides its high level of amino acid homology (75%) with the Na,K-ATPase, the colonic H,K-ATPase also shares a common pharmacological profile with Na,K-ATPase, because both are ouabain-sensitive and Sch 28080-insensitive. These features raise the possibility that an unrecognized property of the colonic H, K-ATPase would be Na+ translocation. To test this hypothesis, ion-selective microelectrodes were used to measure the intracellular Na+ activity of X. laevis oocytes expressing various combinations of P-ATPase subunits. The results show that expression in oocytes of the colonic H,K-ATPase affects intracellular Na+ homeostasis in a way similar to the expression of the Bufo marinus Na,K-ATPase; intracellular Na+ activity is lower in oocytes expressing the colonic H,K-ATPase or the B. marinus Na,K-ATPase than in oocytes expressing the gastric H,K-ATPase or a beta subunit alone. In oocytes expressing the colonic H,K-ATPase, the decrease in intracellular Na+ activity persists when diffusive Na+ influx is enhanced by functional expression of the amiloride-sensitive epithelial Na+ channel, suggesting that the decrease is related to increased active Na+ efflux. The Na+ decrease depends on the presence of K+ in the external medium and is inhibited by 2 mM ouabain, a concentration that inhibits the colonic H,K-ATPase. These data are consistent with the hypothesis that the colonic H,K-ATPase may transport Na+, acting as an (Na,H),K-ATPase. Despite its molecular and functional characterization, the physiological role of the colonic (Na,H),K-ATPase in colonic and renal ion homeostasis remains to be elucidated.

Animals↗
PubMed1997

Symmetric pH dependence of buffering power in giant fused cells from frog kidney proximal tubule.

This study measures the intrinsic buffering power (beta(i)) of giant fused cells from the proximal kidney tubule of the frog (Rana ridibunda) as a function of intracellular pH (pHi). We monitored pHi and transmembrane potential difference during acid or alkaline cell loading, achieved by removal of NH4Cl-containing solutions or CO2-HCO3(-)-equilibrated solutions, respectively, in the absence of extracellular Na+. Data were well fit by the equation for a single, monoprotic buffer with a maximum beta(i) at a pHi of 7.39 +/- 0.06 and a total buffer concentration of 30.7 +/- 1.6 mM (means +/- SD). From pHi measurements obtained during CO2-HCO3- exposure, we also calculated the buffering power afforded by the CO2-HCO3- pair, and we show its increasing contribution to total buffering power at increasing PCO2 and pHi. To our knowledge, this is the first report of a cell type in which intrinsic cell buffers can be adequately approximated as a single monoprotic buffer with a negative logarithm of apparent dissociation constant in the normal physiological range and essentially symmetric dependence on pHi in both acid and alkaline ranges.

Ammonium Chloride↗
PubMed1996

Further investigation of ionic diffusive properties and of NH4+ pathways in Xenopus laevis oocyte cell membrane.

To study the ionic diffusive properties and the NH4+ pathways in the Xenopus laevis oocyte cell membrane, we recorded the effects of various inhibitors on membrane potential (Vm) and membrane resistance (Rm); intracellular acidification was taken as an index of NH4+ influx from the bath to the cytoplasm. The following results were obtained: in the control state, barium and quinine (Q) ions depolarized Vm and raised Rm, consistent with inhibition of K+ conductance(s). Diphenylamine-2-carboxylic acid (DPC), 3',5'-dichlorodiphenylamine-2-carboxylic acid (DCDPC) and gadolinium ions hyperpolarized Vm and increased Rm, suggesting the inhibition of nonselective cationic conductance(s). In the presence of 20 mmol/l NH4Cl, Vm depolarized, Rm fell, and intracellular pH (pHi) decreased, consistent with an NH4+ influx. In the presence of DPC, the same manoeuvre induced a biphasic Vm change (i.e. a spike depolarization followed by a membrane hyperpolarization) and a fall of Rm; in most oocytes, intracellular acidification persisted and was reversible upon adding ouabain (Oua). These results indicate that a DPC-sensitive conductance is not the unique NH4+ pathway and that Na, K-ATPase may also mediate NH4+ influx. However, Oua did not prevent the Rm decrease, suggesting that ouabain-insensitive rheogenic pathway(s) are activated. Thus, we investigated the Vm change induced by NH4Cl addition in the presence of DPC: the spike depolarization followed by secondary hyperpolarization became a plateau depolarization when Q was added, suggesting involvement of Q-sensitive pathway(s) in the above described biphasic Vm change. In the presence of DPC, Q and Oua, intracellular acidification upon adding NH4Cl persisted consistent with further NH4+ influx through quinine-, DPC- and Oua-insensitive pathway(s).

Animals↗