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Biomedical subjects

A Mimran

Publications and source records attributed to A Mimran.

At least 145 records · Page 8Linked to original sources
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

Reversal of acute renal failure following percutaneous transluminal recanalization of an atherosclerotic renal artery occlusion.

Thrombosis of the renal artery to a single functioning kidney is a known cause of anuric acute renal failure in atherosclerotic hypertensive patients. In the present report, recovery of renal function rapidly occurred following transluminal recanalization of the occluded artery with a 7F catheter after a 5-week period of anuria. The most interesting feature was that improvement of renal artery permeability was observed following a minimal interventional procedure.

Acute Kidney Injury↗
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

[Effects of sodium depletion in rats actively immunized against renin].

The influence of active immunization against renin on systolic blood pressure in response to a dietary sodium restriction was assessed in normotensive rats (WKY) and spontaneously hypertensive rats (SHR). Immunization was obtained by multiple injections of pure submaxillary murine renin. Animals received a normosalt diet (NS diet) for 6 days. Then sodium was abruptly removed from the diet (LS diet), and rats were maintained for an additional 6 day-period on this salt-free diet. In rats maintained on NS diet, immunization induced a decrease in systolic blood pressure (SBP) about 11 p. 100 and 27 p. 100 respectively in WKY immune and SHR immune groups. SBP was not affected by abrupt dietary sodium removal in non-immunized rats from both strains. However, in immunized rats sodium restriction was accompanied by a significant SBP decrease compared to the value observed during NS period in the same group. The relative variation in SBP was about 10 p. 100 and 14 p. 100 respectively in WKY immune and SHR immune groups. The present study shows that active immunization against renin leads to a reduction in systolic blood pressure regardless to the initial pressure level. When sodium is removed from the diet, systolic blood pressure level is maintained in non-immunized rats, whereas it decreases in immunized rats of both strains. These results confirm the importance of an efficient renin-angiotensin system in the adaptative response to sodium restriction.

Animals↗
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

Renal function in hypertension.

Hypertension certainly accelerates the age-related changes in renal structure and function, mainly in the glomerulus. Both sodium handling and the renin-angiotensin system are involved in the aging process. Among the available classes of antihypertensive agents, the eventual deterioration of renal function induced by angiotensin-converting enzyme inhibitors in bilateral stenosis and stenosis of a single functioning kidney suggests that changes in glomerular pressure may participate in the changes of renal function. In essential hypertension and other conditions, it is possible that at a certain stage an increase in intraglomerular capillary pressure plays a role in the acceleration of the loss in renal function. As a consequence, it is proposed that in treating hypertension we should aim at reducing systemic blood pressure together with an attempt to reduce intraglomerular pressure using agents that act predominantly on post-glomerular resistance in order to have renal protection.

Acute Kidney Injury↗
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↗
PubMed1988

Contrasting effects of captopril and nifedipine in normotensive patients with incipient diabetic nephropathy.

Microalbuminuria is a reliable predictor of the eventual development of overt diabetic nephropathy and blood pressure is known to accelerate the course of this nephropathy. In the present studies, the effect of a 6-week treatment by placebo (n = 7), nifedipine (n = 7) and captopril (n = 8) on renal function and urinary excretion of albumin (UAE) was investigated in normotensive, insulin-dependent, diabetic patients with incipient nephropathy (UAE greater than 15 micrograms/min). No change in arterial pressure, renal function or UAE was observed in the placebo group. In response to captopril and nifedipine, mean arterial pressure decreased slightly and similarly in both groups. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) increased to a similar extent in the nifedipine group, thus resulting in no change in filtration fraction (FF). In response to captopril, GFR was unchanged whilst ERPF increased; as a consequence FF decreased. Opposite changes in UAE were observed in response to the two treatments; UAE decreased by 40% in the captopril group and by 40% in nifedipine-treated patients. These results indicate that intrarenal changes may be crucial with respect to the effect of therapy on UAE. It is suggested that only agents which reduce FF and probably intraglomerular capillary pressure, such as converting enzyme inhibitors, alter UAE and may possibly interfere with the course of incipient diabetic nephropathy in normotensive patients.

Adolescent↗
PubMed1988

Nicardipine and atrial natriuretic factor increase whole body vascular permeability in rats.

Using binephrectomized anaesthetized rats, we explored the possibility that calcium antagonists may alter the partition of extracellular fluid between plasma and the interstitium, as suggested for atrial natriuretic factor (ANF). The effects of intravenous infusion of synthetic ANF (103-126 ANP; Wy 47.663) and the dihydropyridine derivative nicardipine were assessed by measuring changes in haematocrit and plasma proteins. After a 40-min infusion of ANF or nicardipine, haematocrit increased significantly (9% and 5.4%, respectively). The calculated loss of plasma volume was 15% after administration of ANF and 9.1% after nicardipine compared with 3.9% in rats receiving vehicle only. Plasma proteins increased by only 3.9% (after ANF) and 3.7% (after nicardipine), less than expected for a plasma volume contraction without protein extravasation. Atrial natriuretic factor and nicardipine induced a similarly slight change in mean arterial pressure. These results suggest that nicardipine and ANF both reduce plasma volume by an extrarenal mechanism; part of the fluid shift might be facilitated by an increased vascular permeability to proteins.

Animals↗
PubMed1988

Effects of captopril and nitrendipine on the response to acute volume expansion in essential hypertension.

The systemic and renal responses to normal volume expansion (1800 ml isotonic saline infused over 3 h) were assessed in 23 patients with essential hypertension after 4-7 days' administration of a placebo or the calcium antagonist nitrendipine (20 mg three times a day) or the angiotensin converting enzyme (ACE) inhibitor captopril (50 pressure mg three times a day). Each drug treatment was associated with a fall in blood pressure of the same magnitude. Treatment with captopril was associated with a significant volume dependence of blood pressure and a blunting of the exaggerated natriuresis of hypertension (71 +/- 16 on placebo and 47 +/- 12 mmol/3 h on captopril; P less than 0.01). Treatment with nitrendipine did not affect the change in blood pressure associated with volume expansion, but significantly enhanced the natriuretic response to volume expansion (61 +/- 8 on placebo and 90 +/- 16 mmol/3 h on nitrendipine; P less than 0.01). No alterations in baseline or volume expansion-induced changes in the glomerular filtration rate or in plasma renin activity were observed during treatment with nitrendipine. Therefore, the exaggerated natriuresis of essential hypertension was blunted by the ACE inhibitor and enhanced by the calcium antagonist, despite a similar reduction in pre-expansion arterial pressure.

Adult↗