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Biomedical subjects

A Mimran

Publications and source records attributed to A Mimran.

At least 181 records · Page 10Linked to original sources
PubMed1986

[Hypertension and stenosis of the graft artery: effects of conversion enzyme inhibition].

The use of angiotensin converting enzyme inhibitors may lead to reversible renal insufficiency in transplant patients with transplant renal artery stenosis (TRAS). We assessed acute effects of captopril (50 mg, p. os) in 7 cadaver kidney recipients (mean age: 35.6 +/- 4 yrs) with TRAS, 9 to 46 mo after transplantation. All patients were treated by prednisolone and azathioprine. After captopril administration, mean arterial pressure decreased from 127 +/- 6 to 119 +/- 7 mmHg, effective renal plasma flow from 152 +/- 19 to 118 +/- 19 ml/min/1.73 m2, glomerular filtration rate from 59 +/- 8 to 39 +/- 10 ml/min/1.73 m2 and filtration fraction from 0.39 +/- 0.02 to 0.32 +/- 0.07. Among the 7 patients, 2 developed immediate and transient anuria; 4 presented a net decrease of GFR, only one had stable GFR. This patient was chronically treated by captopril; as BP was not controlled, furosemide (40 mg p. os) was added. Serum creatinine increased from 180 to 250 mumol/l. Percutaneous angioplasty was done without decrease in BP; however, treatment by captopril and furosemide could be reinstitued without deterioration in renal function. We conclude that: acute renal failure in kidney graft recipients with TRAS is frequent, but not mandatory; sodium depletion induced by diuretics enhances the fall in GFR; acute effect of captopril must be assessed in patients with TRAS before the use of this product as long term antihypertensive treatment.

Acute Kidney Injury↗
PubMed1986

[Effect of inhibition of angiotensin converting enzyme on hypertension following kidney transplantation].

The activation of the renin angiotensin system is thought to be an important factor contributing to hypertension following kidney transplantation (TX). We studied 21 hypertensive renal transplant recipients, without evidence of acute graft rejection or transplant artery stenosis, 6 to 60 months post-TX. The acute responses of mean arterial pressure (MAP) and renal hemodynamics (ERPF: effective renal plasma flow, 131I-Hippuran clearance) and function (GFR: glomerular filtration rate, creatinine clearance; UNaV: urinary sodium excretion rate) to converting enzyme inhibition (CEI) by captopril were assessed. CEI induced a decrease in MAP (118 +/- 2 to 110 +/- 2 mmHg), renal resistance (RR: 0.27 +/- 0.02 to 0.21 +/- 0.01) and filtration fraction (FF: 0.31 +/- 0.02 to 0.23 +/- 0.01). ERPF (307 +/- 24 to 333 +/- 18 ml/min/1.73 m2) and GFR (88 +/- 5 to 78 +/- 5 ml/min/1.73 m2) were not significantly changed. UNaV increased by 53 +/- 24 mumol/min. Changes in MAP (r = -0.66), ERPF (r = 0.74) and FF (r = -0.88) were significantly correlated with the log of control plasma renin activity (PRA). In 10 patients with an increase of ERPF (range: + 30 to + 70%) and no change in GFR, the activated renin system could originate from the recipient's own kidneys. In the remaining 11 patients, CEI was associated with no increase in ERPF (change: + 2 to - 27%) and a fall in GFR, a response suggesting a possible intrarenal vascular damage. These results indicate that RAS participates in the regulation of systemic and renal vascular tone, with a possible predominant effect on efferent glomerular arteriole.

Adult↗
PubMed1985

Effect of chronic nifedipine in patients inadequately controlled by a converting enzyme inhibitor and a diuretic.

Nifedipine, in a slow release preparation, was given at a mean daily dosage of 47 +/- 4 mg to 12 patients with severe hypertension in whom arterial pressure was not satisfactorily controlled (mean arterial pressure 132 +/- 4 4 mm Hg) by the combination of a converting enzyme inhibitor and a diuretic. The addition of nifedipine induced an appreciable decrease in mean arterial pressure of 31 +/- 5 mm Hg and of serum potassium and plasma aldosterone. After adequate control of hypertension and because of severe hypokalemia in some patients, discontinuation of the diuretic was attempted in 10 subjects. After 1.7 +/- 0.5 months of treatment by the converting enzyme inhibitor and nifedipine no change in arterial pressure occurred while serum potassium had returned to normal in most patients. These results show that nifedipine may be useful in patients with a residual rise of arterial pressure when treated by converting enzyme inhibitor plus diuretics; in such patients, however, the serum potassium concentration should be carefully monitored. In addition, our observations suggest that calcium blockers may be an effective alternative to diuretics in patients receiving a converting enzyme inhibitor.

Adult↗
PubMed1985

Recovery of renal function in patients with accelerated malignant nephrosclerosis on maintenance dialysis with management of blood pressure by captopril.

Recovery of renal function to a self-sustaining level was observed in 4 patients with accelerated malignant hypertension who required chronic hemodialysis therapy. Excellent blood pressure control was achieved in all the patients on captopril therapy. Hemodialysis could be discontinued after 2-9 months of captopril therapy; on recovery of renal function levels of creatinine clearance became stable ranging from 28 to 56 ml/min within 5-15 months of captopril treatment, and remained at this level during 21-64 months of observation. The management of hypertension and the inhibition of the renin-angiotensin system afforded by chronic angiotensin-converting enzyme inhibition is very promising as a means of reversing the process of malignant nephrosclerosis.

Adolescent↗
PubMed1985

Renal effects of calcium blockade by tiapamil in normal and hypertensive subjects.

The acute hypotensive and renal effects of the calcium antagonist tiapamil, a verapamil derivative, were studied in nine normal and 13 essential hypertensive subjects undergoing water diuresis. Tiapamil decreased mean arterial pressure slightly in normotensive subjects and more markedly in hypertensive patients (-6 +/- 1 versus -10 +/- 2%). The effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) were unaffected in both groups. A striking natriuresis was observed selectively in the hypertensive group (+344 +/- 84 versus +42 +/- 22 mmol/min) and was associated with an increase in the calculated fractional distal delivery of sodium and uric acid excretion rate. Plasma aldosterone concentration decreased moderately and to the same extent in both groups. In conclusion, tiapamil induced a marked natriuresis in essential hypertensive patients, despite a decrease in blood pressure, and in the absence of renal vasodilatation; this may suggest the existence in essential hypertension of a calcium-linked abnormality in the renal proximal tubular handling of sodium.

Adult↗
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↗
PubMed1985

Renin angiotensin aldosterone system, urinary prostaglandins and kallikrein in pregnancy induced hypertension. Evidence for a disregulation of the renin-angiotensin-prostacyclin loop.

Plasma renin activity and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and four prostaglandins (PGE2, PGF2 alpha, 6 keto PFG1 alpha and TXB2) in 23 patients with pregnancy induced hypertension (17 with permanent PIH and six with labile PIH, since in these latter their hypertension was controlled only by home bed rest) and in 16 normotensive pregnant women at the same stage of gestation (31 +/- 3 weeks). PRA was lower in permanent PIH than in controls and in labile PIH. No difference between the three groups was observed for plasma aldosterone and the urinary excretion of kallikrein and of the prostaglandins except that TXB2 was higher in labile PIH than in permanent PIH. Correlation studies of kallikrein disclosed correlations with most prostaglandin excretions, explained by the physiological stimulation of phospholipase A2 by kallidin. Correlation studies of PRA disclosed unexpected negative correlation with PGE2 and 6 keto PGF1 alpha in the permanent PIH group. In conclusion, labile PIH has a different biological profile than permanent PIH since they have higher PRA and higher TXB2 excretion, an association which suggests a more pronounced ureteral compression by the gravid uterus in this group. Permanent PIH has a disregulation of the renin angiotensin-prostacyclin loop since PRA and 6 keto PGF1 are negatively correlated. This suggests the role of an independent vasopressive substance which would stimulate PGI2 and suppress renin secretion.

Female↗
PubMed1985

[Acute effect of nifedipine on arterial pressure and the renin-angiotensin system in healthy subjects and hypertensives].

The acute effects of nifedipine (20 mg capsules) on the blood pressure and renin-angiotensine system were studied in 108 subjects, 25 normotensives, 51 borderline hypertensives and 33 permanent essential hypertensives. The fall in mean blood pressure (MBP) was rapid (less than 30 minutes) and significant in all groups; the amplitude the hypotensive response expressed as a percentage of the basal MBP was directly related to the basal MBP value (r = 0.54, p less than 0.001). The amplitude of the response correlated with the control plasma renin activity only the group with permanent hypertension (r = - 0.40, p less than 0.025). The fall in blood pressure and the reflex sympathetic stimulation induced by nifedipine were not associated with an increased plasma renin activity. The plasma aldosterone concentrations varied only in the group of permanent hypertensive patients after nifedipine ( - 4 +/- 1 ng/dl, p less than 0.01).

Adolescent↗
PubMed1984

Renal adaptation to sodium deprivation. Effect of captopril in the rat.

Dietary sodium restriction is associated with a rapid decrease in urinary sodium excretion and achievement of a new sodium balance within three to five days. In addition, renal vasoconstriction and progressive activation of intrarenal systems with vasoconstrictor (renin-angiotensin) or vasodilating (kallikrein-kinin and prostaglandins) properties are observed. The relationship between sodium homeostasis and the renin-angiotensin system was assessed through the use of captopril in the rat. Treatment with captopril, before and during a six-day period after suppression of dietary sodium, was associated with sodium wasting (urinary sodium always exceeded sodium intake during the observation period); in addition, the normal increase in urinary aldosterone was blunted by about 80 percent. When captopril treatment was given for six days to rats maintained on long-term sodium restriction (at least four weeks) urinary sodium increased, although transiently; at the end of the study, renal vasodilatation together with a redistribution of glomerular blood flow to nonsuperficial glomeruli was observed. These studies indicate that captopril administration markedly blunts the renal and systemic adaptations to a reduced sodium intake in the rat. They suggest that the renin-angiotensin system is probably indispensable in preventing sodium loss when dietary sodium is suppressed.

Adaptation, Physiological↗
PubMed1984

Effect of converting enzyme inhibition by enalapril on sodium homeostasis in the rat.

The effect of oral treatment with the converting enzyme inhibitor enalapril on sodium homeostasis was investigated in the rat. Treatment by enalapril prior to and during a 6 day period following abrupt suppression of dietary Na+ was associated with a sodium wasting state (urinary Na+ always exceeded intake during the observation period) and blunting by 90% of the aldosterone response to Na+ restriction In rats on chronic low Na+ intake, enalapril produced a slight, transient natriuresis together with a marked increase in drinking volume. In Na+ replete rats, enalapril had no influence on sodium balance. Converting enzyme inhibition markedly impaired the systemic and renal response to Na restriction and enalapril had no natriuretic effect in the Na+ replete state.

Administration, Oral↗
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↗
PubMed1984

[Renal response to acute expansion of the extracellular volume in renal transplant patients].

The response to acute isotonic saline loading (1 800 ml in 3 hours) was assessed in 12 normotensive and 11 hypertensive renal transplant recipients. Both groups had similar renal function, daily urinary excretion of sodium and doses of steroids. The natriuretic response to saline was not affected in hypertensive transplants and changes in blood pressure, renin and aldosterone were identical in both groups. Similar correlations between pre-saline fractional excretion of sodium (FENa+) and the FENa+ obtained during saline were obtained in normotensive and hypertensive patients. These results demonstrate that in renal transplant recipients of young donors no exaggeration of the response to saline occurs in hypertensive subjects thus suggesting that normal kidneys may carry their characteristics when transplanted in a new environment. The role of renal denervation remains unclear.

Adult↗
PubMed1984

[Pseudohyperaldosteronism induced by alcohol-free aniseed aperitif in alcoholic cirrhotic patients].

The authors report 2 cases of pseudohyperaldosteronism secondary to consumption of alcohol-free "pastis" in abstinent alcoholic cirrhotics. In both cases patients presented with ascites, edema, increased blood pressure and hypokalemic alkalosis. Except for hypokalemia, the disorders improved rapidly after withdrawal of the beverage. Glycyrrhizic acid, present in little amounts in the beverage, is presumably responsible for this syndrome. Patients with alcoholic cirrhosis would be particularly at risk. It is suggested that alcohol-free "pastis" could be responsible for ascites and edema in cirrhotic patients. This drinking habit should be looked for in abstinent cirrhotic patients with ascites, particularly in case of associated systemic hypertension.

Beverages↗
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↗