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N Caron

Publications and source records attributed to N Caron.

At least 19 recordsLinked to original sources
PubMed2006

Ferrofluidic adaptive mirrors.

A magnetic liquid mirror based on ferrofluids was demonstrated. Magnetic liquid mirrors represent a major departure from solid mirror technology. They present both advantages and disadvantages with respect to established technologies. Stroke (from a fraction of a wave to several hundreds of micrometers), cost (a few dollars per actuator), and scalability (hundreds of thousands of actuators) are the main advantages. Very large mirrors having diameters of the order of a meter should be feasible. There are a few disadvantages. The most important disadvantage is the time response, which is of the order of a few milliseconds. Although this time response could be further decreased with additional technical developments, it is unlikely to match the speed of solid mirrors. The technology is still in its infancy, and considerable work must still be done. However, the advantages are such that the technology is worth pursuing.

Journal Article↗
PubMed2006

Increased renal vascular reactivity to ANG II after unilateral nephrectomy in the rat involves 20-HETE.

This study examined the role of intrarenal ANG II in the renal vascular reactivity changes occurring in the remaining kidney undergoing adaptation following contralateral nephrectomy. Renal blood flow responses to intrarenal injections of ANG II (0.25 to 5 ng) were measured in anesthetized euvolemic male Wistar rats 1, 4, 12, and 24 wk after uninephrectomy (UNX) or sham procedure (SHAM). At week 4, renal vasoconstriction induced by 2 ng ANG II was greater in UNX (69 +/- 5%) than in SHAM rats (50 +/- 3%; P < 0.01). This response was inhibited, by 50 and 66%, and by 20 and 25%, in SHAM and UNX rats, after combined injections of ANG II and losartan, or PD-123319 (P < 0.05), respectively. Characteristics of ANG II receptor binding in isolated preglomerular resistance vessels were similar in the two groups. After prostanoid inhibition with indomethacin, renal vasoconstriction was enhanced by 42 +/- 8% (P < 0.05), only in SHAM rats, whereas after 20-HETE inhibition with HET0016, it was reduced by 53 +/- 16% (P < 0.05), only in UNX rats. These differences vanished after concomitant prostanoid and 20-HETE inhibition in the two groups. After UNX, renal cortical protein expression of cytochrome P-450 2c23 isoform (CYP2c23) and cyclooxygenase-1 (COX-1) was unaltered, but it was decreased for CYP4a and increased for COX-2. In conclusion, renal vascular reactivity to ANG II was significantly increased in the postuninephrectomy adapted kidney, independently of protein expression, but presumably involving interactions between 20-HETE and COX in the renal microvasculature and changes in the paracrine activity of ANG II and 20-HETE.

Adaptation, Physiological↗
PubMed2004

Changes in renal haemodynamics induced by indomethacin in the rat involve cytochrome P450 arachidonic acid-dependent epoxygenases.

A significant renal vasodilation was observed previously after an acute cyclo-oxygenase (COX) inhibition induced with indomethacin. Because this effect could be due to COX-dependent intrarenal metabolization of arachidonic acid through cytochrome P450 (CYP450) pathways, the aim of the present study was to investigate, in vivo, possible interactions between COX and CYP450 mono-oxygenases. Mean arterial pressure (MAP) and renal blood flow (RBF), using an electromagnetic flow transducer for RBF evaluation, were measured continuously in 71 anaesthetized euvolaemic rats. Appropriate solvents (vehicle), 3 mg/kg indomethacin, 17-octadecynoic acid (17-ODYA; 2 mmol/L), either miconazole (MI; 1.5 mmol/L) or N-methylsulphonyl-6-(2-propargyloxyphenyl)hexanamide (MS-PPOH; 5 mg/kg) and N'-hydroxyphenylformamidine (HET0016; 5 or 10 mg/kg) were administered to inhibit either COX, CYP450 mono-oxygenases, epoxygenases or hydroxylase, respectively. The CYP450 and COX inhibitors were also combined as follows: 17-ODYA/indomethacin, MI (or MS-PPOH)/indomethacin, HET0016/indomethacin and indomethacin/HET0016. Mean arterial pressure and RBF were not modified by vehicle, 17-ODYA or MI (or MS-PPOH). However, MAP decreased slightly (P < 0.05; paired t-test, 5 d.f.) and RBF increased transiently (P < 0.05; anova, 5 d.f.) after HET0016. In contrast, MAP decreased by 10 mmHg (P < 0.05) and RBF increased by 10% (P < 0.05) after indomethacin. This enhancement was prevented by 17-ODYA or MI (or MS-PPOH), but not by HET0016. Moreover, RBF increased step-wise to 21% in the indomethacin/HET0016 experiment (P < 0.05). Consequently, changes from baseline in renal vascular resistance differed among treatments, averaging -2 +/- 3 (vehicle), -13 +/- 3 (indomethacin; P < 0.05 vs vehicle), -4 +/- 3 (17-ODYA/indomethacin), -3 +/- 4 (MI or MS-PPOH/indomethacin), -15 +/- 3 (HET0016/indomethacin; P < 0.05) and -22 +/- 4% (indomethacin/HET0016; P < 0.05). In conclusion, these results demonstrate that the renal vasodilation induced by indomethacin can be prevented by prior inhibition of CYP450 mono-oxygenases and further suggest that the CYP450 epoxygenases pathway may prevail.

Animals↗
PubMed2001

Stimulation of DNA repair by the spermatidal TP1 protein.

The chromatin remodeling process that takes place during spermiogenesis in mammals is characterized by a transient increase in DNA single-strand breaks (SSB). The mammalian transition proteins (TPs) are expressed at a high level at mid-spermiogenesis steps coincident with chromatin remodeling and could be involved in the repair of these lesions since SSB are no longer detected in terminally differentiated spermatids. We report that TP1 can stimulate the repair of SSB in vitro and demonstrate that in vivo repair of UV-induced DNA lesions is enhanced in mammalian cells stably expressing TP1. These results suggest that, aside from its role in DNA compaction, this major transition protein may contribute to the yet unidentified enzymatic activity responsible for the repair of SSB at mid-spermiogenesis steps. These results also suggest that the TP1 proteins have the potential to participate in the repair process following genotoxic insults and therefore may play an active role in the maintenance of the integrity of the male haploid genome during spermiogenesis.

Animals↗
PubMed2001

Endothelin resets renal blood flow autoregulatory efficiency during acute blockade of NO in the rat.

Renal blood flow (RBF) autoregulatory efficiency may be enhanced during NO inhibition in the rat, as recently reported. Under these conditions, endothelin (ET) synthesis and release may be increased. Our purpose was therefore to determine the role of ET in RBF autoregulatory changes induced by NO inhibition. To address this point, ET(A/B) receptors were blocked in anesthetized rats with bosentan, or selectively with BQ-610 or BQ-788. NO synthesis was inhibited with N(G)-nitro-L-arginine methyl ester (L-NAME). Mean arterial pressure (MAP) was decreased after bosentan (-10 mmHg; P < 0.01) or increased after L-NAME (25 mmHg; P < 0.001). RBF measured with an electromagnetic flow probe was reduced by L-NAME (-50%) and by BQ-788 (-24%). The pressure limits of the autoregulatory plateau (P(A) approximately 100 mmHg) and of no RBF autoregulation (P(o) approximately 80 mmHg) were significantly lowered by 15 mmHg after L-NAME but were unchanged after bosentan, BQ-610, or BQ-788. During NO inhibition, autoregulatory resetting was completely hindered by bosentan (P(A) approximately 100 mmHg) and by ET(B) receptor blockade with BQ-788 (P(A) approximately 106 mmHg), but not by ET(A) receptor blockade with BQ-610 (P(A) approximately 85 mmHg). These results suggest that the involvement of ET in the RBF autoregulatory resetting occurs during NO inhibition, possibly by preferential activation of the ET(B) receptor. However, the relative contribution of ET receptor subtypes remains to be further specified.

Angiotensin Receptor Antagonists↗
PubMed2000

Comparative study of the coupling between topoisomerase I activity and high-mobility group proteins in E. coli and mammalian cells.

It is now well established that the HMG box DNA-binding motif can alter the topology of double-stranded DNA in several ways. Using the spermatid-specific tsHMG as a model protein of the HMG-1/-2 family, we have demonstrated that its expression in E. coli produces an increase in plasmid supercoiling density that is likely a consequence of its ability to constrain free supercoils in vivo. As demonstrated in vitro, stabilization of free DNA supercoils by tsHMG prevents topoisomerase I from gaining access to the template and could represent a mechanism for the apparent inhibition of topoisomerase I in bacteria. A similar modulation of eukaryotic topoisomerase I activity was not detected after expression of the tsHMG in mammalian cells. This differential response is discussed in terms of the marked difference in DNA packaging and accessibility of free supercoils in prokaryotic vs. eukaryotic cells.

Cell Line↗
PubMed2000

Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat.

In cultured vascular muscle cells, nitric oxide (NO) has been shown to inhibit voltage-dependent Ca(2+) channels, which are involved in renal blood flow (RBF) autoregulation. Therefore, our purpose was to specify in vivo the effects of this interaction on RBF autoregulation. To do so, hemodynamics were investigated in anesthetized rats during Ca(2+) channel blockade before or after acute NO synthesis inhibition. Rats were treated intravenously with vehicle (n = 10), 0.3 mg/kg body wt N(G)-nitro-L-arginine-methyl ester (L-NAME; n = 7), 4.5 microg. kg body wt(-1). min(-1) nifedipine (n = 8) alone, or with nifedipine infused before (n = 8), after (n = 8), or coadministered with L-NAME (n = 10). Baseline renal vascular resistance (RVR) averaged 14.0 +/- 1.2 resistance units and did not change after vehicle. RVR increased or decreased significantly by 27 and 29% after L-NAME or nifedipine, respectively. Nifedipine reversed, but did not prevent, RVR increase after or coadministered with L-NAME. RBF autoregulation was maintained after L-NAME, but the autoregulatory pressure limit (P(A)) was significantly lowered by 15 mmHg. Nifedipine pretreatment or coadministration with L-NAME limited P(A) resetting or suppressed autoregulation at higher doses. Results were similar with verapamil. Intrarenal blockade of Ca(2+)-activated K(+) channels also prevented autoregulatory resetting by L-NAME (n = 8). These findings suggest NO inhibits voltage-dependent Ca(2+) channels and thereby modulates RBF autoregulatory efficiency.

Animals↗
PubMed1999

Amplification by atrial natriuretic peptide of the haemodynamic and renal responses to an acute volumic stress in the rat.

1. The purpose of the present study was to test the effects of synthetic atrial natriuretic peptide (ANP) on renal haemodynamics and excretory capacities of salt and water in the rat during an 'acute volumic stress', which was induced by brisk disturbances of the circulatory volume. 2. To this end, 29 anaesthetized male Wistar rats were rapidly injected with 1 mL of 0.85% NaCl, repeated twice at 60 s intervals. The injectates contained no ANP (n = 5) or 1 x 0.25 (n = 6), 3 x 0.25 (n = 6), 1 x 2.5 (n = 6) or 3 x 2.5 micrograms (n = 6) ANP, added to the first injectate only (1 x) or to each injectate (3 x). Renal blood flow (RBF) was continuously measured with an electromagnetic flow transducer. 3. Renal blood flow increased transiently (approximately 30 s) by approximately 13% (P < 0.05) during each injection of saline without ANP. Addition of 0.25 or 2.5 micrograms ANP to the first injectate enhanced RBF by 21 and 35%, respectively (both P < 0.05), but did not modify the time sequence. Furthermore, addition of 0.25 microgram ANP to the second and third injectate produced an almost similar change in RBF at the end of each injection (delta RBF = 20 and 17%, respectively). In contrast, the addition of 2.5 micrograms ANP to the second and third injectate did not produce the same changes in RBF observed at the end of the first injection. The amplitude of the change in RBF was then similar to the increase in RBF induced by 1 mL saline without ANP. Mean arterial pressure (MAP) did not change significantly during repeated injections of saline alone or with addition of 0.25 microgram ANP to the first injectate. However, MAP decreased significantly (by 5, 9 and 9 mmHg) after the injection of 3 x 0.25, 1 x 2.5 or 3 x 2.5 micrograms ANP, respectively. 4. Sodium excretion was rapidly increased from 2.600 +/- 0.654 to 9.330 +/- 1.322 mumol/min after injection of 3 x 1 mL of 0.85% NaCl (P < 0.05). Thereafter, sodium excretion remained enhanced throughout the experiment, so that 70% of the sodium load injected was recovered at the end of the experiment. Atrial natriuretic peptide added to the injectates further elevated the maximal responses in diuresis and natriuresis induced by saline injections without ANP (P < 0.001). A maximal effect was observed after the addition of 2.5 micrograms ANP to the first saline solution. When the amount of sodium excreted was calculated by integrating the areas under the curve of the natriuretic responses, a relationship was established as a function of the amount of ANP added to the saline solutions. It was characterized by a threshold in the presence of 2.5 micrograms ANP added to the first injectate when the integration period was limited to 4 min 30 s and 14 min 30 s after starting the first injection of the varying test solutions. When the integration period was extended until the end of the experiment (2 h), the amount of sodium excreted in each group was further enhanced, especially after injection of 3 x 1 mL of 0.85% NaCl without ANP or with 1 x 0.25 and 3 x 0.25 microgram ANP. Differences in sodium excretion between groups were attenuated (P < 0.054, ANOVA). 5. In conclusion, our results demonstrate differential effects of synthetic ANP on renal vascular reactivity and excretory capacity. These effects were superimposed on changes induced by acute volumic stress. In particular, effects of saline injections on renal vascular compliance were amplified in the presence of ANP added in varying amounts to the injectates. This amplification was limited to 2.5 micrograms ANP.

Animals↗
PubMed1999

Measurement of changes in glomerular filtration rate induced by atrial natriuretic peptide in the rat kidney.

This study was undertaken to improve the measurement of glomerular filtration rate (GFR) during the acute diuretic phase induced by atrial natriuretic peptide (ANP), which may indeed alter the renal clearance of inulin (GFRCL) due to dead space error. A technique to measure GFR without urine collections was therefore developed in anaesthetized rats prepared as for micropuncture. To do so, arterial blood was periodically collected and renal venous blood was withdrawn simultaneously from a catheter inserted into the left suprarenal vein to determine the renal extraction coefficient of inulin (CEIN). In addition, renal blood flow (RBF) was continuously measured with an electromagnetic flow transducer fitted around the left renal artery to estimate renal plasma flow (RPF). GFR (GFRCE) was then calculated as the product of RPF and CEIN. To study the effects of ANP on GFR, rats were injected i.v. with 10 microliters of saline without (n = 6; vehicle) or with 1 microgram ANP (n = 6; ANP) and GFRCE and GFRCL were compared before and after each treatment. They did not differ significantly during baseline measurements in each experimental group and were not modified after vehicle. Similarly, RBF remained constant. In contrast, RBF and GFRCE increased rapidly and simultaneously 90 s after ANP, from 9.07 +/- 0.25 to 10.07 +/- 0.35 (12%) and from 1.209 +/- 0.188 to 1.715 +/- 0.190 ml min-1 (42%), respectively (P < 0.05). GFRCL increased to an even greater extent (88%). Moreover, the peak enhancement of GFRCL was delayed and occurred 180 s after ANP. The renal clearance of inulin was thus unduly elevated due to sudden changes in the dead space induced by the diuretic effect of ANP. In conclusion, determination of glomerular filtration rate by the method of renal extraction of inulin provided more reliable results than those achieved using the classical method of renal clearance of inulin. Moreover, it was sufficiently sensitive to detect small and transient changes in GFR induced by the injection of 1 microgram ANP.

Animals↗
PubMed1998

Architectural DNA-binding properties of the spermatidal transition proteins 1 and 2.

Mammalian spermiogenesis is characterized by replacement of somatic histones by a set of basic nuclear transition proteins thought to be actively involved in the chromatin remodeling process. The two major transition proteins of the elongating spermatids, namely TP1 and TP2, were expressed and purified using a bacterial expression system. Both topoisomerase and ligase-mediated supercoiling assays demonstrated that TP1, as well as TP2, did not produce detectable changes in the twist and/or writhe of DNA molecules upon binding. Ligase-mediated circularization assay further demonstrated that neither of the transition proteins under study produced bends in linear DNA but that they both have the capacity to stimulate oligomerization of linear DNA fragments. We further established that the transition proteins are in vitro substrates for the Ca+2-phospholipid-dependent protein kinase (PKC) as well as the cAMP-dependent protein kinase (PKA). PKC phosphorylation was found to strongly weaken the DNA-condensing ability of TP2. These results suggest that the major transition proteins represent architectural factors able to stabilize DNA in a nonsupercoiled state, thereby promoting DNA condensation.

Amino Acid Sequence↗
PubMed1997

Differential effects of sulindac on renal hemodynamics and function in the rat.

Renal hemodynamics were studied using an electromagnetic perivascular flow sensor in anesthetized rats injected i.v. with vehicle, 5 or 10 mg/kg body weight (b.w.) sulindac. No hemodynamic changes occurred with vehicle (n = 6), but mean arterial pressure was significantly decreased (by 15 mmHg) with sulindac (n = 12). In the 5 mg/kg b.w. sulindac group (n = 7), renal blood flow progressively and significantly increased from 7.88 +/- 0.36 to 8.98 +/- 0.58 ml/min, except during concomitant intrarenal infusion of 3 mg/kg b.w. per h proadifen (n = 7). The pressure limits for efficient and no renal blood flow autoregulation remained unchanged (approx. 100 and 80 mmHg, respectively). In the 10 mg/kg b.w. sulindac group (n = 5), renal blood flow did not change but autoregulatory pressure limits were lowered by 10 mmHg 2 h after treatment (P < 0.025). Also, Na+ retention was marked. Prostanoid excretion in urine was significantly reduced with either dose but basal plasma renin activity was not (about 8 ng/ml per h; n = 15). When plasma renin activity was enhanced after a reduction in renal perfusion pressure (n = 21), it was decreased from 11.5 +/- 1.2 to 7.4 +/- 0.2 ng/ml per h only by 10 mg/kg b.w. sulindac (P < 0.05; n = 6). In conclusion, differential effects of sulindac on renal hemodynamics, Na+ excretion and plasma renin activity were demonstrated. Renal hemodynamic changes could be related in part to the cytochrome P-450 arachidonic acid pathway.

Animals↗
PubMed1996

Medium aperture meso-caval shunts reliably prevent recurrent variceal hemorrhages.

BACKGROUND: Objectives of partial medium aperture mesocaval shunts (MCS) include reduction of portal hypertension to prevent recurrent variceal hemorrhage, preservation of portal flow through liver while maintaining an intact porta hepatis to facilitate a future liver transplant (OLTx). PATIENTS AND METHODS: Fifteen patients were retrospectively analyzed to review the indications for the procedure, its short- and long-term complications as well as patency and functional status of the shunt. They were followed for a period of 21 months. RESULTS: The perioperative and long-term mortality rate was 0%. Rebleeding rate perioperatively and in follow-up was 0%. Early shunt nonfunction was 13% and post-shunt encephalopathy (PSE) was 20%. The encephalopathy was grade I to II and controlled medically. Abdominal ultrasound and Doppler confirmed 13 patent shunts (2 patients did not agree to ultrasound) with preserved hepatopetal flow in 10. CONCLUSIONS: Medium aperture MCS utilizing ringed polytetrafluoroethylene (PTFE) grafts safely and reliably prevent recurrent variceal hemorrhage. Encephalopathy is infrequent and mild. This technique preserves the portal venous anatomy making a future OLTx technically easier.

Adult↗
PubMed1995

Renal hemodynamics and blood flow autoregulation during acute cyclooxygenase inhibition in male rats.

After the acute inhibition of prostanoid synthesis, adjustments of renal hemodynamics may not be characterized immediately. Therefore, time-related effects of indomethacin on hemodynamics and renal blood flow (RBF) autoregulation were studied in anesthetized euvolemic male rats injected intravenously with vehicle, indomethacin (3, 4, or 5 mg/kg body wt), or meclofenamate (4 or 5 mg/kg body wt). Hemodynamics and RBF autoregulation were not influenced by vehicle injection, nor by time (n = 6). In contrast, mean arterial pressure (MAP) decreased significantly from 117 +/- 4 to 103 +/- 3 mmHg, and RBF progressively and significantly increased from 8.00 +/- 0.34 to 9.17 +/- 0.50 ml/min in the 3 mg/kg body wt indomethacin group (n = 8). Treatment with the higher doses of indomethacin (n = 9) or meclofenamate (n = 6) did not change RBF, while MAP decreased by 15 mmHg. A time-dependent significant enhancement of RBF autoregulatory efficiency was found in the drug-treated rats. Changes in renal function and reductions of prostanoid excretion in urine, of plasma renin activity, or serum aldosterone were similar in the nonsteroidal antiinflammatory drug groups. In conclusion, our findings demonstrate important time-related adjustments of renal hemodynamics in male rats treated with indomethacin, especially with the lower dose (3 mg/kg body wt iv). The factor(s) responsible for the hemodynamic changes remains unknown.

Aldosterone↗
PubMed1994

[Atrial natriuretic factor and water-sodium homeostasis: concepts and perspectives].

The discovery of an endocrine activity of the heart in 1981 was fundamental in order to understand the regulation of the effective circulatory volume. Indeed, the hormone which is secreted by the atrial cells (ANF) when these are distended suddenly in the presence of an enhanced preload of the heart, acts very rapidly upon the kidneys and the vasomotor tone. Its action restores without delay the effective circulatory volume following the renal elimination of an appropriate fraction of salt and water and attenuates the pressor effects of the increased intravascular volume. In this regard, the hormone is an emergency mediator. ANF may also be a long-term regulator of salt and water homeostasis by modulating the renal excretion of sodium. Finally, its role in pathological conditions such as congestive heart failure or essential hypertension remains to be elucidated. Nevertheless, interesting therapeutic perspectives may be considered, based on the unusual inactivation of ANF by clearance receptors.

Atrial Natriuretic Factor↗
PubMed1988

Comparison between pentobarbital- and muscimol-induced feeding in satiated sheep.

Twenty sheep were used to study the mechanisms by which the intracerebral administration of pentobarbital and of muscimol induces feeding in ruminants. Injections of 1 mumol calcium induced a weak feeding response at 1 h postinjection compared with control values (108 vs. 63 g, p less than 0.05). Injections of 78 mumol pentobarbital and of 100 nmol muscimol elicited strong feeding responses (p less than 0.01). A preinjection of 1 mumol calcium reduced the response to pentobarbital by about 40% but did not affect the response to muscimol. Administration of 1.1 mmol sodium chloride reduced the effect to pentobarbital by about 60% but only partially decreased the effect to muscimol. Administration of picrotoxin, a GABA antagonist, slightly decreased the feeding response to pentobarbital and to muscimol. Administration of gamma-vinyl GABA, an inhibitor of the enzyme GABA transaminase, did not affect feeding behavior of sheep at any of the doses tested (0-10 mumol). Injections of gamma-vinyl GABA followed by equimolar injections of GABA failed to provoke any feeding response. The data suggest that pentobarbital and muscimol may induce feeding by acting on a similar hypothalamic receptor complex but by different mechanisms. The lack of effect of GABA itself remains unexplained.

Aminocaproates↗
PubMed1980

Cyclophosphamide potentiation and aldehyde oxidase inhibition by phosphorylated aldehydes and acetals.

Fourteen phosphorylated acetals and aldehydes were synthesized for testing in vitro as inhibitors or substrates of aldehyde oxidase, an enzyme involved in the conversion of aldophosphamide to inactive carboxyphosphamide, and for concurrent in vivo administration with cyclophosphamide to mice bearing L1210 ascites tumor cells. Five phosphorus derivatives gave Ki values of 0.1--0.3 mM compared to 0.03 mM for pyridoxal, as determined in aldehyde oxidase assays using N-methylnicotinamide as the substrate. The most active phosphorus inhibitor, ethyl phenyl(2-formylethyl)phosphinate (2b), and pyridoxal were further shown to give competitive and mixed inhibition, respectively. Three aldehydes, administered concurrently with cyclophosphamide, produced greater increases in life span of L1210-implanted mice than did pyridoxal. All four agents gave an average increase in life span greater than 50% over that shown by cyclophosphamide alone.

Acetals↗
PubMed1978

[Electra 600 d : results of a three year study (author's transl)].

Electra 600 D has been used in our laboratory for 3 years. The Quick's prothrombine time is the only test routinely performed with satisfactory results. The measure of activated partial thromboplastin time, the assays of factor II, factor V and complex VII + X are unsatisfactory, probably because of the type of the reagents which are used.

Autoanalysis↗