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Biomedical subjects

J Ribstein

Publications and source records attributed to J Ribstein.

At least 91 records · Page 5Linked to original sources
PubMed1990

[Comparison of pro-edematous effects of 2 calcium antagonists in bilaterally nephrectomized rats].

Chronic treatment with dihydropyridines and to a lesser extent other calcium antagonists often cause peripheral edema without fluid retention. To test the possibility that calcium antagonists affect extracellular fluid partition between plasma and interstitium, we compared the effects of a benzothiazepine derivate diltiazem, a dihydropyridine derivate nicardipine and vehicle in binephrectomized anesthetized rats by measuring changes in hematocrit and plasma protein concentration. Forty minutes infusion of low dose of nicardipine and diltiazem (0.1 and 10 micrograms/kg/min respectively) had no significant effect on blood pressure (-2 +/- 2 and -4 +/- 3% respectively); nicardipine increased hematocrit by 5.6 +/- 0.5% (p less than 0.05); while diltiazem had no significant effect as compared to the vehicle (+1.5 +/- 0.3 and +1.5 +/- 0.3% respectively). The calculated loss of plasma volume during nicardipine infusion was 9.2 +/- 0.8% as compared to 2.5 +/- 0.6% and 2.7 +/- 0.6% in rats receiving diltiazem and vehicle respectively. Infusion of higher doses of nicardipine and diltiazem (1 and 100 micrograms/kg/min respectively) decreased blood pressure by 21 +/- 2 and 19 +/- 2% while the changes in hematocrit were not different than those observed with with the lower doses (5.5 +/- 0.6 and 1.4 +/- 0.3% respectively). To document and localize an alteration in vascular leak of proteins induced by the drugs, albumin-bound Evans Blue (EB) extravasation was measured spectrophotometrically in different tissues after extraction by formamide. Nicardipine but not diltiazem increased vascular permeation of EB-albumin in skeletal and cardiac muscle. No change was observed in brain, liver, spleen as compared to rats receiving the vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1990

[Myocardial morphological changes related to sodium intake in normotensive and hypertensive patients never treated before].

Several factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) and LV structure in 30 normotensive (NT) subjects aged 34 +/- 11 years (mean +/- SD) and 50 patients (39 +/- 10 years) with mild essential hypertension EH (canal blood pressure 154 +/- 16/96 +/- 11 mmHg), who had never received antihypertensive drugs. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and urinary sodium excretion (UNa, mmol/24h) was taken as an index of sodium intake. In NT and EH, LVM was directly correlated with UNa (r = 0.48 and 0.49; p less than 0.006 and 0.002, respectively). A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, and body weight in the two groups. In NT the correlation with UNaV was the result of an increase of the end-diastolic diameter without change in PWT whilst in EH it was the consequence of an increase in wall thickness (R = 0.49, p less than 0.0001) without a modification of LV diameter. These results suggest that salt intake may be an important determinant of cardiac structural adaptation in both NT and EH subjects; however, only EH have a salt sensitive LV wall hypertrophy.

Adult↗
PubMed1990

[Left ventricular mass and glomerular hyperfiltration in essential hypertension].

OBJECTIVE: to assess the early involvement to target organs in never treated essential hypertensives (HT). METHODS: effective renal plasma flow (ERPF, 131I-Hippurate) and glomerular filtration rate (GFR, 99mTc-DTPA) were estimated in 80 mild HT. Left ventricular mass (LVM, M-mode echocardiography), sodium intake (24h UNaV) and urinary kallikrein (Kall) were also measured. Hyperfiltering patients (HF, GFR = 155 +/- 3 ml/min: 1.73 m2, n = 21) were defined by comparison with age-matched normotensive. HF patients were pair-matched for age, sex and blood pressure level with normofiltering hypertensives (NF, GFR = 112 +/- 3, n = 21). RESULTS: are expressed as mean +/- sem [table: see text] CONCLUSION: These results suggest that a high Na intake is associated with hyperfiltration and higher LVMI in subjects with never treated essential hypertension of short duration.

Adult↗
PubMed1990

[Suppression of the immediate pressive response to unilateral nephrectomy by atrial natriuretic peptide in the rat].

Unilateral nephrectomy (UNX) is associated with an immediate and transient increase in arterial pressure and in prompt natriuresis from the remaining kidney. The hypothesis that atrial natriuretic peptide (ANP) is involved in the acute adaptation to unilateral nephrectomy was tested in euvolemic anesthetized Sprague-Dawley rats. In a first series of experiments, an increase in circulating ir-ANP levels (from 23.5 +/- 3.6 to 66.3 +/- 12.8 fmol/ml; p less than 0.01) was found within 2 minutes following renal exclusion. In a second set of experiments, the ANP response was inhibited by performing a right atrial appendectomy, in order to eliminate the major source of ANP, or by intravenous administration of monoclonal antibodies directed against ANP. When UNX was performed in the control groups (sham atrial appendectomy and administration of non specific monoclonal antibodies), mean arterial pressure rose immediately (maximal about 12% within 4 minutes) and transiently (return to pre-UNX values within 20 minutes) after UNX. At the same time, central venous pressure, monitored in the right atrium, tended to decrease slightly. In rats pretreated by right atrial appendectomy or by monoclonal antibodies directed against ANP, arterial pressure increased to the same extent as observed in control groups; this increase however was significantly more prolonged. In control groups, urinary cGMP excretion, the biological marker of ANP, increased twofold in parallel with the natriuretic response. These two responses were blunted in right atrial appendectomized rats and in rats receiving antibodies against-ANP. These results suggest that atrial natriuretic peptide plays a major role in the immediate functional adaptation to unilateral nephrectomy by blunting the increase in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The renin-angiotensin system and renal function in kidney transplantation.

The use of converting enzyme inhibitors (CEI) has permitted us to assess the role of the renin-angiotensin system in the control of arterial pressure and renal function in various conditions. In renal transplant recipients treated by azathioprine and steroids, the occurrence of CEI-induced deterioration of renal function is highly suggestive of renal artery stenosis, whereas renal vasodilatation associated with unchanged glomerular filtration rate in response to CEI is indicative of a significant role of native kidneys. In hypertensive recipients without renal artery stenosis, the absence of renal hemodynamic changes after CEI may be predictive of subsequent chronic rejection. The information provided by CEI is rather different in cyclosporine treated subjects. In this setting, no acute effect of CEI on renal hemodynamics is detectable. Whether the renal response to CEI is similar in cyclosporine when compared to conventionally treated patients with renal artery stenosis remains to be demonstrated.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Sodium intake influences the effects of atriopeptin on blood pressure and transcapillary fluid shift in the rat.

The influence of chronic changes in sodium intake on the acute effects of atrial natriuretic peptide (ANP) on arterial pressure and fluid translocation was assessed in acutely binephrectomized rats. After 3 weeks of either low sodium or high sodium diet, animals were administered ANP at doses of 0.1 and 1 microgram/kg/min. A marked and irreversible hypotensive response to ANP was observed with the higher infusion rate in the low sodium group, whereas blood pressure did not change significantly in the other groups. The effect of ANP on plasma protein concentration was less marked than that on hematocrit in all groups and was not significantly affected by sodium intake. The effect of both doses of ANP on hematocrit was enhanced in the high sodium group, indicating that the fluid shift out of the intravascular compartment was magnified by high sodium intake.

Animals↗
PubMed1989

Effect of cyclosporine on blood pressure and renal function of recent type 1 diabetes mellitus.

The effect of cyclosporine A therapy on blood pressure and renal function was assessed in 11 young adults with type 1 diabetes of recent onset (7 +/- 1 weeks). Metabolic control and renal haemodynamics and function were evaluated at 3-month intervals before, during and after cessation of a 6-month course of cyclosporine A (initial dose 7.5 mg/kg per day, then adapted on whole-blood trough levels of 401 +/- 45 and 308 +/- 49 ng/ml at 3 and 6 months, respectively). A significant increase in blood pressure (from 117 +/- 2/65 +/- 2 to 122 +/- 2/72 +/- 3 mmHg; P less than 0.01) and a decrease in 99Tc-DTPA (diethylene triaminepentaacetic acid) clearance (124 +/- 6 to 98 +/- 5 ml/min per m2; P less than 0.01) were observed after 3 months of cyclosporine A; both alterations remained unchanged after 6 months. No variation in body weight, 24-h urinary sodium or urinary albumin excretion was observed. Blood pressure and the glomerular filtration rate returned to basal levels 3 months after the cyclosporine A therapy ceased. These results suggest that even moderate doses of cyclosporine A have a reversible deleterious effect on blood pressure and renal function in young diabetic patients.

Adolescent↗
PubMed1989

Influence of sodium intake on left ventricular structure in untreated essential hypertensives.

Among the many factors that have been implicated in the pathogenesis of myocardial hypertrophy is a sodium effect. In the present study, the influence of dietary sodium, estimated by 24-h natriuresis, on left ventricular mass was assessed in 41 patients with mild essential hypertension who had never been treated. Posterior wall thickness and left ventricular mass, but not left ventricular internal diameter were directly correlated with 24-h natriuresis (r = 0.47 and 0.46; P less than 0.02 and 0.002, respectively). Stepwise multiple regression analysis confirmed that 24-h natriuresis was a determinant of left ventricular mass independently of sex, age, body weight, blood pressure and the duration of hypertension. These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives.

Adolescent↗
PubMed1989

Effect of nicardipine and atriopeptin on transcapillary shift of fluid and proteins.

The possibility that calcium antagonists may alter extracellular fluid partition, as already suggested for atrial natriuretic peptide (ANP), was explored in anephric anesthetized rats by measuring changes in hematocrit and plasma proteins during infusion of synthetic ANP-(103-126) and the dihydropyridine derivative nicardipine. In response to ANP (1 micrograms.kg-1.min-1) or nicardipine (0.1 microgram.kg-1.min-1), which had a similar effect on arterial pressure, hematocrit increased by 9 +/- 0.1 and 5.4 +/- 0.3%, respectively, whereas plasma protein concentration increased to a lesser extent (3.9 +/- 0.3 and 3.7 +/- 0.2%, respectively). The simultaneous infusion of ANP and nicardipine had no additive effect on hematocrit, whereas the effect on arterial pressure was markedly enhanced. In additional experiments, an attempt was made to estimate the vascular leak of albumin in various tissues, using a quantitative Evans blue technique. Both ANP and nicardipine increased dye extravasation in skeletal and cardiac muscle, whereas ANP but not nicardipine increased extravasation in intestine. No significant change was observed in brain, liver, and lungs. These results suggest that nicardipine and ANP reduce plasma volume by an extrarenal mechanism. This fluid shift, possibly resulting from hemodynamic changes at the capillary level, is associated with a marked transfer of plasma albumin out of the vascular compartment.

Animals↗
PubMed1989

Contrasting effects of acute angiotensin converting enzyme inhibitors and calcium antagonists in transplant renal artery stenosis.

Deterioration of renal function is a major concern during treatment by converting enzyme inhibitors of hypertensive kidney recipients with transplant renal artery stenosis. However, there has been no assessment of the frequency of this complication and its specificity for converting enzyme inhibitors as compared to other antihypertensive drugs. The effect of acute administration of captopril on mean arterial pressure, glomerular filtration rate (GFR) (creatinine clearance) and effective renal plasma flow (clearance of 131I-hippuran) was assessed in eight hypertensive patients with transplant renal artery stenosis. Captopril induced a decrease in mean arterial pressure (128 +/- 6-121 +/- 7 mmHg) and a reduction in GFR (59 +/- 8-44 +/- 8 ml/min per 1.73 m2, P less than 0.05). The decrease in GFR was observed in seven out of eight patients and varied between 0% and 100% of the pre-captopril value. Effective renal plasma flow was maintained (157 +/- 47-141 +/- 24 ml/min per 1.73 m2) and filtration fraction decreased by 15 +/- 7%. The effect of captopril was compared to that of nifedipine (N = 20 mg) in four patients. Despite a larger decrease in mean arterial pressure (130 +/- 7-109 +/- 10 mmHg), no reduction in GFR was observed (68 +/- 13-71.4 +/- 8). Effective renal plasma flow was unchanged and filtration function slightly increased. Surgical or percutaneous transluminal angioplasty in five patients suppressed the captopril-induced decrease in GFR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Renal response to acute volume expansion in primary hyperaldosteronism].

The exaggerated natriuretic response to extracellular fluid volume expansion (VE) observed in essential hypertension (EH) is related directly to blood pressure (BP) and indirectly to plasma renin activity (PRA). In order to evaluate the precise role of different hormonal parameters, the response to acute VE (isotonic saline, 1,800 ml IV over 3 hours) was assessed in 14 patients with primary aldosteronism (PA, surgically proven adrenal adenoma) and 18 clinically matched EH. At the time of the maneuver, BP and sodium intake were similar in the two groups, but serum potassium (2.89 +/- 0.13 vs 3.69 +/- 0.09 mmol/l), PRA (0.9 +/- 0.2 vs 3.5 +/- 0.9 ng/ml/h) and plasma aldosterone concentration (PAC, 25.9 +/- 3.8 vs 12.6 +/- 1.6 ng/dl) were significantly different. During VE, sodium excretion (UNaV) increased more in PA than in EH (98.1 +/- 15.2 vs 63.5 +/- 7.9 mmol/3 h); moreover, the slope of the regression line relating UNAVVE to UNaVcontrol was significantly steeper in PA. By contrast, the change in BP and indices of VE (hematocrit and plasma protein concentration) as well as the decrease in PRA (-45 +/- 9 vs -43 +/- 5 p. 100) and the increase in ANP (+ 65 +/- 16 vs + 69 +/- 28 p. 100) were similar in the two groups. VE left PAC unchanged in PA, whilst it decreased PAC in EH. We conclude that the natriuretic response to volume expansion is more marked in primary aldosteronism than in essential hypertension, a difference which is not explained by variations in the renin-angiotensin system or atrial natriuretic peptide.

Female↗
PubMed1989

[Determinants of left ventricular hypertrophy in hypertensive subjects that have never been treated: role of the sodium intake].

Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) in 41 patients aged 38 +/- 10 (mean +/- SD) with mild essential hypertension (casual blood pressure 149 +/- 17/91 +/- 11 mmHg). Patients had never been given antihypertensive drugs before and ingested ad libitum sodium intake. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and sodium intake was estimated from urinary sodium excretion rate (UNa, mmol/24h). Both PWT and LVM, and not telediastolic diameter or LV fractional shortening, were directly correlated with UNa (r = 0.47 and 0.46; p less than 0.02 and 0.002, respectively. A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, body weight, blood pressure and duration of hypertension. No correlation was found between LVM and plasma renin activity, whilst a positive one existed between PWT and hematocrit (r = 0.42; p less than 0.007). These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives, possibly in expanding volume or activating the adrenergic system.

Cardiomegaly↗
PubMed1989

[Liquid transfers induced by a calcium antagonist and the atrial natriuretic peptide in binephrectomized rats].

Peripheral edema without fluid retention is a common side effect of treatment with calcium antagonists (CA). The possibility that CA may alter extracellular fluid partition between plasma and interstitium, as suggested for atrial natriuretic peptide (ANP) was explored in binephrectomized anesthetized rats by measuring changes in hematocrit and plasma protein concentration during infusion of synthetic 103-126 ANP (Wy 47.663) and the dihydropyridine derivate nicardipine. After a forty minutes infusion of ANP (1 microgram/kg/mn), hematocrit and plasma protein increased 9.1 +/- 0.3 and 3.9 +/- 0.3 p. 100 respectively; the calculated loss of plasma volume during ANP infusion was 14.5 +/- 1.1 p. 100 as compared to 3.9 +/- 0.6 p. 100 in rats receiving vehicle only. Infusion of nicardipine at 1 microgram/kg/mn increased hematocrit by 5.7 +/- 0.2 p. 100 (corresponding to a 9.1 +/- 0.9 p. 100 decrease in plasma volume), and plasma proteins by 3.7 +/- 0.2 p. 100. To document and localize an alteration in vascular leak of proteins induced by the drugs, albumin-bound Evans blue (EB) extravasation was measured spectrophotometrically in different tissues after extraction by methyl-formamide. Both ANP and nicardipine increased vascular penetration of EB-albumin, mainly in skeletal and cardiac muscle; no changes was observed in brain, liver, spleen as compared to rats receiving the vehicle; ANP but not nicardipine increase EB-albumin permeability in intestine. These results suggest that nicardipine as well as ANP reduce plasma volume by increasing vascular leak of fluids and macromolecules.

Animals↗
PubMed1989

Angiotensin converting enzyme inhibitors and renal function.

Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. However, acute renal deterioration may occur in some conditions where angiotensin plays a crucial role in the regulation of the glomerular filtration rate (GFR), such as volume depletion, severe stenosis of both renal arteries and stenosis of the renal artery of a single functioning kidney. Acute renal failure induced by ACE inhibition may develop without a reduction in systemic blood pressure it is enhanced by prior sodium depletion and is reversible when treatment is withdrawn. The relative superiority of ACE inhibitors in slowing the progression of chronic parenchymal renal disease remains to be demonstrated, although promising results have been reported in patients with diabetic nephropathy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

[Arterial hypertension, renal function and angiotensin-converting enzyme inhibition].

Several effects of the antihypertensive treatment with angiotensin converting-enzyme inhibitors (ACEI)--whether beneficial or detrimental--are best explained at the renal level. In the presence of a renal artery stenosis, the activation of the intrarenal renin-angiotensin system is first directed at maintaining glomerular filtration and intracapillary hydrostatic pressure through post-glomerular vasoconstriction. Long-term elevation of blood pressure is associated with a shift of the renal function curve, possibly linked with an alteration of the intrarenal renin-angiotensin system. Inhibition of the converting enzyme does affect the mechanisms of sodium conservation. In a subset of essential hypertensive subjects, ACEI may correct a subtle primary abnormality in modulation by sodium of renal (and adrenal) response(s) to angiotensin. Finally, the possibility of renal protection in circumstances such as diabetes mellitus, provides an exciting area of investigations for antihypertensive treatment with ACEI.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Contrasting acute effects of captopril and nifedipine on renal function in renovascular hypertension.

In order to assess the determinants of renal function deterioration induced by angiotensin-converting enzyme inhibition (ACEI) in renovascular hypertension, studies were performed in patients with bilateral stenosis (BS; n = 12) and stenosis of a solitary kidney (SK; n = 10). Acute administration of captopril was associated with a consistent fall in glomerular filtration rate in 5 of 12 patients with BS and 8 of 10 with SK. Overall, glomerular filtration rate decreased by 22 +/- 7%, while mean arterial pressure decreased by only 8 +/- 2% and renal plasma flow remained unaltered. The ACEI-induced change in glomerular filtration rate was unrelated to blood pressure or basal plasma renin activity, but it was inversely related to pre-ACEI filtration fraction. In a comparative study conducted in 6 BS and 4 SK patients, acute administration of nifedipine was associated with a change in glomerular filtration rate of 13 +/- 5% and no change in renal plasma flow, despite a marked decrease in mean arterial pressure of 19 +/- 4%. In contrast, in the same patients, glomerular filtration rate fell by 23 +/- 12%, renal plasma flow did not change and mean arterial pressure fell slightly by 7 +/- 3% after ACEI.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗