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H Boulanger

Publications and source records attributed to H Boulanger.

8 recordsLinked to original sources
PubMed1998

[Hypercalciuria].

Hypercalciuria is a very frequent disorder that is defined by a daily calcium excretion rate in excess of 0.1 mmol/kg. Whatever its mechanism, it always expresses an increased input of calcium in extracellular fluid, from intestine and (or) bone. In few instances, hypercalciuria is secondary to an underlying disease that needs to be identified (primary hyperparathyroidism, cancer, granulomatosis...). However, in most cases, it is a primary (idiopathic) disorder that reveals an abnormal handling of calcium by intestinal and renal tubular epithelia. It is then treated by a restricted dietary supply in sodium and animal proteins, and by the use of thiazide diuretics.

Absorption↗
PubMed1997

Apical location and inhibition by arginine vasopressin of K+/H+ antiport of the medullary thick ascending limb of rat kidney.

To characterize and localize a K+/H+ antiport mechanism in the renal medullary thick ascending limb (MTAL), membrane vesicles were isolated from a rat MTAL homogenate. K+/H+ antiport (in > out H+ gradient-stimulated 86Rb+ uptake) was abolished by barium and verapamil (apparent Ki of 55 microM) but unaffected by other K+ channel blockers such as quinidine and high amiloride concentrations. SCH 28080, a H+/K+-ATPase blocker, did not affect K+/H+ antiport. K+/H+ antiport activity was correlated positively with the enrichment factor of the membranes in the apical marker enzyme alkaline phosphatase (r = 0.875, p < 0.01) and negatively correlated with the enrichment factor in basolateral Na+/K+-ATPase (r = -0.665, p < 0.05). Moreover, a functional interaction occurred with Na+/H+ exchange (NHE) consistent with colocation of K+/H+ antiport and apical NHE-3, not basolateral NHE-1. K+/H+ antiport was shown by intracellular pH measurements to be inhibited by arginine vasopressin and 8-bromo-cAMP through cAMP-dependent protein kinase (protein kinase A) activation. These results demonstrate the presence of a K+/H+ antiport mechanism, which is inhibited by arginine vasopressin via protein kinase A, in the apical membrane of the MTAL.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

[Role of nitric oxic in pregnancy and pre-eclampsia].

The mechanisms involved in the physiology of pregnancy and in the pathophysiology of preeclampsia are still largely unknown. Prostaglandins metabolism, especially an imbalance between thromboxane A2 and prostacyclin does not appear sufficient to explain all the observed changes. Recent studies have shown that nitric oxide (NO), a vasodilating and a platelet anti-aggregating factor, could play a pivotal role in inducing hemodynamic changes during pregnancy. NO is produced in excess during pregnancy, mainly in uterine and renal vascular beds. Similarly, NO is in part responsible for the non-responsiveness of the vessels to vasoactive agents and plays a relevant role in peripheral vasodilation and in lowering systemic blood pressure. Furthermore, NO improves blood supply to the fetal-placental unit and to maternal kidneys. An impaired NO metabolism in pregnant rats induces changes similar to those observed in human preeclampsia. NO pathway represents a new approach to the physiology of pregnancy and to the pathophysiology of preeclampsia. Moreover, NO donors might be carefully proposed as new therapeutic agents in this disorder.

Animals↗
PubMed1997

[Pefloxacin as a first-line treatment for nephrotic syndrome in minimal glomerular lesions in the adult. Multicenter study of 32 patients].

Minimal change nephrotic syndrome (MCNS) is the most frequent single cause of nephrotic syndrome occurring both in adults and children. Although it appears to be a self-limiting disorder (10% spontaneous remissions within the fortnight following the initial flare), MCNS displays a high rate of complications during the nephrotic period (10 to 15% cases) and prompts one to treat patients as early as possible. Corticosteroids are currently used as first-line treatment. A 16 weeks full-dose steroid course (1 mg/kg/day) usually induces remission in 75% MCNS in adults. Nevertheless, duration of treatment (9 months) and occurrence of relapses despite a slowly tapering dosage schedule, expose patients to steroids side-effects. Immunosuppressive drugs are recommended in case of steroid resistance and their side-effects are not harmless. Therefore, an alternative to steroids or immunosuppressives would lend a serious helping hand in MCNS management. The present work is dealing with pefloxacin efficacy in 40% MCNS in adults. Thirty-two MCNS adult patients were treated in a national multicenter study. A short-duration pefloxacin course (4 to 6 weeks) allowed partial or complete remission in 13 out of 32 cases. Thus far, this effect was undescribed for this class of drugs. Pefloxacin belongs to antibacterial agents of the fluoroquinolone family and is active against Gram negative Enterobacteria species. Fluoroquinolones also act on eukaryotic cells as lymphocytes and chondrocytes and alter IL2, gamma IFN and integrin expression. Although their precise mode of action is unknown in this kind of immunological disorder, fluoroquinolones might represent an alternative to steroids in some adult form of MCNS. However, predictive criteria for sensitivity to fluoroquinolones are currently not available and further controlled studies would be helpful using fluoroquinolones as first-line treatment in all the MCNS.

Adolescent↗
PubMed1996

Lack of beneficial effects on the NO-donor, molsidomine, in the L-NAME-induced pre-eclamptic syndrome in pregnant rats.

1. In pregnant rats, chronic NO-synthase inhibition induces the development of a pre-eclamptic syndrome, characterized by an increase in maternal blood pressure, a loss of vascular refractoriness to pressor stimuli, a reduction in litter size and a decrease in pups (and maternal) weight. We investigated whether a NO-donor, molsidomine, administered during NO synthase inhibition, could restore a normal pregnancy. 2. Pregnant rats were given daily, starting from day 14 of gestation, saline (controls), or L-NAME (50 mg kg-1 d-1), or molsidomine (15 or 30 mg kg-1 d-1), or the L-NAME + molsidomine combinations. Maternal blood pressure and body weight, litter size, pups weight and vascular reactivity to pressor stimuli (angiotensin II, noradrenaline, electrical stimulation of the spinal cord) were investigated. 3. L-NAME alone, as compared to controls, increased maternal blood pressure, reduced litter size (-59%), increased foetal reabsorptions (+ 625%) and decreased foetal weight (-10%). Vascular reactivity to pressor stimuli was enhanced. 4. Molsidomine alone, as compared to controls, dose-dependently decreased maternal blood pressure but had no effect vascular reactivity and, whatever the dose, on foetal outcome. 5. The L-NAME-molsidomine combinations dose (of molsidomine)-dependently limited the rise in maternal blood pressure induced by L-NAME alone but unexpectedly, dose-dependently and significantly worsened pregnancy evolution, e.g., at 30 mg kg-1 d-1: litter size (-80%), foetal reabsorptions (+ 1025%), foetal weight (-24%). Vascular reactivity to pressor stimuli was paradoxically further enhanced. 6. Thus, in a chronic NO deprivation-induced model of pre-eclampsia in rats, molsidomine, possibly because of its hypotensive action, worsens the foetal outcome, which questions the usefulness of NO-donors in pre-eclamptic women.

Animals↗