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Biomedical subjects

M Dupont

Publications and source records attributed to M Dupont.

At least 73 records · Page 4Linked to original sources
PubMed1985

Role of vasopressin in cardiovascular adaptation to sodium depletion in the conscious rat.

The hypothesis that vasopressin participates in cardiovascular adaptation to sodium depletion was examined in male Sprague-Dawley rats studied after 6 days (n = 28) or 4 weeks (n = 28) of low sodium diet. Blood pressure was similar on the two diets but heart rate, water intake and urine volume were all significantly greater at 4 weeks. Animals were randomly assigned to four acute treatment groups: controls, vasopressin pressor antagonist, d(CH2)5Tyr(Me)AVP (AVPA, 10 micrograms/kg); angiotensin converting enzyme (ACE) inhibitor, enalaprilic acid (150 micrograms/kg); combined ACE inhibitor and AVPA. Cardiac output and blood flow distribution were measured using labelled microspheres. Blood pressure, cardiac output and blood flow distribution were unchanged after AVPA alone. Angiotensin converting enzyme inhibition and ACE inhibitor plus AVPA produced similar falls in mean blood pressure at 6 days (-12 +/- 1, -14 +/- 3 mmHg) and 4 weeks (-11 +/- 2, -16 +/- 2 mmHg) due to parallel falls in peripheral resistance. Angiotensin converting enzyme inhibition was associated with selective increases in renal and mesenteric blood flow. Renal blood flow increased further after combined blockade at 6 days (ACE inhibitor 9.68 +/- 0.71; ACE inhibitor plus AVPA 11.92 +/- 0.73 ml/min per g, P < 0.05) but not at 4 weeks (ACE inhibitor 11.15 +/- 0.23; ACE inhibitor plus AVPA 10.76 +/- 0.78 ml/min per g). Vasopressin appears to contribute to early but not late cardiovascular adaptation to sodium depletion. A specific effect on the renal vascular bed is only revealed after removal of the dominant effect of angiotensin II (ANG II).

Animals↗
PubMed1985

[The renin-angiotensin system and renal adaptation to sodium restriction].

The renin angiotensin aldosterone system (RAAS) is activated during the early phase of renal adaptation to sodium restriction. The effect of the converting enzyme inhibitor (CEI) MK 421 (MK) was studied when administered 3 days before and 6 days after sodium restriction. Mean arterial pressure, variations of urinary aldosterone, renal blood flow and sodium balance were studied. The results are the following; (Formula: see text) Those results demonstrate that CEI is associated with a renal inadaptation to sodium restriction. Other studies demonstrate that this disequilibrium persists during the second week of treatment in the rat. Those results may be related to an inhibition of aldosterone effect during the sodium restriction, a renal vasodilatation or an accumulation of kinin and endogenous prostaglandins. In summary, a functional RAAS is necessary during the functional adaptation to a sodium restriction. The renal prostaglandins stimulation may contribute to the disequilibrium balance in association with the CEI administration.

Adaptation, Physiological↗
PubMed1984

[Clinical value of the estimation of plasma converting enzyme activity].

Plasma angiotensin I-converting enzyme "activity" (CEA) was estimated as its enzymatic effect on the synthetic substrate HHL in normal subjects and patients with untreated sarcoidosis, alcoholic decompensated liver cirrhosis and scleroderma. CEA was above the upper limit of normal in 60% of sarcoidosis cases and 30% of cirrhotics; it was within normal in scleroderma. The assessment of the influence of chloride concentration on CEA showed that maximum was obtained for a concentration of 300 mM. In addition the inhibitory effect of angiotensin I and the converting enzyme inhibitors SQ 14225 and MK 422 was demonstrated together with the action of high concentrations of penicillamine. The inhibitory influence of these substances was similar when added to the plasma of normal or sarcoidosis subjects.

Adult↗
PubMed1984

[Renal adaptation to a restriction of sodium intake in the rat: effects of inhibition of the renin-angiotensin system].

The relationship between sodium homeostasis and the renin-angiotensin system was assessed through the use of two angiotensin-converting enzyme inhibitors (captopril and enalapril) in the rat. Treatment with captopril (group SQ) or enalapril (group MK) before and during a 6-day period of sodium free diet was associated with sodium wasting; on the sixth day of sodium restriction, sodium excretion was 164 +/- 17 and 144 +/- 10 mumol/24 h in SQ and MK group respectively. In addition, the cumulative Na+ excretion during the 6 day period of sodium-free diet was 1.04 +/- 0.07 mmoles in untreated rats and 1.70 +/- 0.13 and 1.86 +/- 0.14 mmoles in MK and SQ group respectively. At the end of the study, mean arterial pressure was lower in treated than in untreated animals. These findings show that in rats both renal and systemic adaptations to reduced sodium intake are markedly impaired by administration of converting enzyme inhibitors.

Adaptation, Physiological↗
PubMed1983

[Pseudo-hypercalcemia of erythrocytic origin. Increased passive membrane permeability to potassium].

Pseudo-hyperkaliemia is a biochemical abnormality suspected when the blood level of K is increased, contrasting with the absence of usual symptoms of hyperkaliemia. The diagnosis is confirmed by the discrepancy between K+ blood levels which are normal if measured immediately after the blood sample is drawn, and increased if the blood sample is incubated at room temperature. In our case, the pseudo-hyperkaliemia is due to the passage of K outside the erythrocytes through increased passive membrane permeability to K. In vivo, this increased passive outflow of K seems to be compensated by an increased active inflow of K dependent on the sodium pump. This explains the absence of true hyperkaliemia and clinical symptoms. In vitro, it seems that the sodium pump is no longer able to ensure this increased activity. Therefore, the abnormality becomes overt, mirrored by a delayed increase in kaliemia.

Adult↗
PubMed1983

Ochronosis: a case report with severe ochronotic arthropathy.

Alkaptonuria is a rare inborn metabolic disorder in which ochronotic pigment is deposited in connective tissue and cartilage. Ochronotic arthropathy is the consequence of longstanding alkaptonuria and leads to progressive joint disability. We report a case of a 67-year old man with severe ochronotic arthropathy involving the spine, the knees, the shoulders and the hips.

Aged↗
PubMed1983

Comparative effects of nifedipine and diltiazem on vascular responses to norepinephrine and angiotensin II.

The effects of nifedipine and diltiazem on renal vascular responses to norepinephrine and angiotensin II were investigated in the isolated blood-free perfused rat kidney. The vasoconstrictor response induced by bolus injections of angiotensin II (5 and 10 ng) and norepinephrine (60, 80 and 100 ng) were assessed before and during perfusion of nifedipine (10(-9) mol l-1 to 10(-6) mol l-1) or diltiazem (3 X 10(-7) mol l-1 to 10(-4) mol l-1). At a concentration higher than 10(-9) mol l-1, nifedipine blunted to a similar extent the responses to both angiotensin II and norepinephrine. At concentrations of 3 X 10(-7) mol l-1 and 10(-6) mol l-1, diltiazem inhibited only the response to angiotensin II without affecting the vasoconstrictor effect of norepinephrine. Increase in diltiazem concentration to 10(-5) mol l-1 and 10(-4) mol l-1 was associated with a similar inhibition of the response to angiotensin II and norepinephrine. These results demonstrate that at concentration less than 10(-5) mol l-1, diltiazem acts as a selective antagonist of the effect of angiotensin II whilst no such selectivity of action was observed with all concentrations of nifedipine used in the present studies.

Angiotensin II↗
PubMed1983

[Histologic and ultrastructural forms of benign tumors of the kidney with renin secretion. Functional implications].

Two cases of renal benign renin-secreting tumours (juxta-glomerular cells tumors) have been compared by optical and electron microscopy. The first is the simplest type of tumoral form which can be observed. This contains secretory cells similar to epitheloid cells of normal juxta-glomerular apparatus, which multiply in well developed arteriolar and capillary network. As in afferent arterioles of glomeruli, transformation of parietal smooth cells in secretory cells can be observed. This results in the presence of intermediate cells, containing both contractile filaments and secretory granules. This tumor does not contain nerves. The second tumor has a more complex structure. Beside usual secretory cells, tubular formations and adrenergic amyelinic nerves are observed. Tubes and nerves have been described separated in many juxta glomerular cells tumors but had never been observed in association. Tubules with small lumen are made of highly dystrophic cells. High concentration of "kallikrein" in tumoral tissue, strongly suggests that they proceed from distal tubule. Unmyelinated nerves from varicosities containing densely cored vesicles characteristics of adrenergic nerves, and synaptic terminal endings on secretory cells. The presence of nerve bundles suggest a nervous regulation of tumoral secretions. This hypothesis is confirmed by dynamic explorations of sympathetic system.

Adult↗
PubMed1983

[Pseudohyperkalemia of erythrocyte origin. Passive increase of membrane permeability to potassium].

The pseudo-hyperkalemia is a biochemical abnormality suspected when the blood level of K is increased, contrasting with the absence of usual symptoms of hyperkalemia. The diagnosis is confirmed by the discrepancy between K+ blood levels which are normal if measured immediately after the blood sample is drawn, and increased if the blood sample is incubated at the room temperature. In our case, the pseudo-hyperkalemia is due to the passage of K outside the erythrocytes by an increased passive membrane permeability to K. In vivo, this increased passive outflow of K seems to be compensated by an increased active inflow of K dependent of the sodium pump. Therefore is explained, the absence of true hyperkalemia and clinical symptoms. In vitro, it seems that the sodium pump is no longer able to assure this increased activity. Therefore the abnormality appears as a late increase of kalemia.

Adult↗
PubMed1982

Evidence for postsynaptic effect of captopril in isolated perfused rabbit kidney.

The influence of captopril (SQ 14225) on the vascular and norepinephrine-releasing responses to nerve stimulation (2, 5 and 10 Hz) was assessed in isolated blood-free perfused rabbit kidney. At a concentration of 0.23 and 0.46 mM in the perfusion medium, captopril markedly attenuated the vasoconstrictor response but did not influence the release of norepinephrine produced by nerve stimulation. These results suggest that captopril may act as an alpha-antagonist at a postjunctional level.

Animals↗
PubMed1982

Scanning electron microscopic study of arterial cushions in rats: a novel application of the corrosion-replication technique.

The morphology and organ distribution of arterial cushions were studied in adult rats (body weight ranging from 200 to 500 gm) by scanning electron microscopic (SEM) observation of corrosion casts. Scanning electron microscopic observations of renal vascular casts were correlated with SEM views of the luminal surfaces of similarly fixed vessels; there was a striking similarity in shape, organ distribution, and dimensions between fixed arterial cushions and indentations at the surfaces of casts. Application of this technique to 11 different organs, some of which had never been studied by SEM before, revealed the occurrence of indentations at branching sites similar to those found in kidneys (and hence they were termed "cushions"). Our findings are in generally good agreement with previous light and transmission electron microscopic studies on rats. Our results support the view that arterial cushions are present throughout the vasculatures of the rat. A quantitative morphologic study of replicated branching sites related to "cushions" showed a great variability of the parent-to-daughter luminal diameter ratio (range 0.87-16.38) and of branching angles. A fruitful application of this technique to other laboratory animals may be anticipated.

Animals↗
PubMed1982

[Arguments in favor of postsynaptic antagonism by captopril (SQ 14,225) in the perfused kidney].

The potential antagonistic effect of high doses of Captopril on renal vascular response to exogenous administration or nerve stimulated release of norepinephrine (NE) was assessed in isolated blood-free perfused rat and rabbit kidneys respectively. At the doses of 0,09 mM and 0,45 mM in rat kidney, captopril blunted significantly the vasoconstrictor effect of exogenous NE (20, 40 and 100 ng) whilst responses to angiotensin II (2,5 and 10 ng) were slightly reduced at the highest dose and responses to serotonin (20, 40 and 100 mg) remained unaffected by either doses of Captopril. The other effective converting enzyme inhibitor, SQ 20881 had no effect on pressor responses to norepinephrine at similar doses. In preliminary rabbit studies, a likewise blunting of pressor effect of exogenous norepinephrine was obtained at the doses of captopril of 0,23 mM and 0,45 mM. Furthermore, these doses of captopril had no effect on either basal or nerve-stimulated NE release whilst nerve-stimulated vasoconstriction was significantly and reversibly blunted at both doses. These studies suggest a) that the inhibitory effect of Captopril on NE renal vasoconstriction in not primarily dependent on converting enzyme inhibition; b) that the observed alpha-antagonistic activity of high doses of captopril occurs principally at a post-junctional level.

Angiotensin II↗