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Biomedical subjects

A Mimran

Publications and source records attributed to A Mimran.

At least 91 records · Page 5Linked to original sources
PubMed1994

Sodium but not chloride ion modulates left ventricular hypertrophy in two-kidney, one clip hypertension.

OBJECTIVE: To assess the role of dietary sodium with or without chloride on the development of hypertension and left ventricular hypertrophy. METHODS AND RESULTS: Forty-nine male Sprague-Dawley rats with two-kidney, one clip hypertension were fed three different diets for 4 weeks after clipping: free access to sodium chloride, sodium citrate or sodium-free diet. Sham-operated rats were used as controls. The final conscious systolic arterial pressure was similar in all hypertensive groups, regardless of diet. A similar increase in left ventricular mass was observed in the rats on the sodium chloride and sodium citrate diets, whereas left ventricular hypertrophy was strikingly attenuated in the rats on the sodium-free diet. CONCLUSION: Dietary sodium restriction prevented the development of left ventricular hypertrophy without affecting consistently the final level of hypertension. Also, the anion associated with sodium had no influence on the level of arterial pressure and left ventricular mass when compared with rats maintained on sodium chloride. It is suggested that dietary sodium itself might be an important modulator of the left ventricular response to hypertension.

Animals↗
PubMed1994

Angiotensin II receptor antagonists versus angiotensin converting enzyme inhibitors: effects on renal function.

PURPOSE: Recent work has suggested that proximal tubular reabsorption of sodium may be regulated by a local renin-angiotensin system which may be independent of the circulating renin-angiotensin system. The aim of this review was to examine the long-term renal consequences of blockade of the renin-angiotensin system by angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists. RESULTS: Except in states of extreme volume depletion, in which ACE inhibitors may, unlike angiotensin II receptor antagonists, have an adverse effect on the glomerular filtration rate, no differences were observed between the two types of inhibitor. Like ACE inhibitors, the angiotensin II inhibitors TCV 116 and losartan cause a marked impairment in the renal adaptation to dietary sodium restriction, suggesting that blockade of the renin-angiotensin system is primarily involved in this process. CONCLUSIONS: Further studies in human renovascular hypertension and chronic renal disease are required.

Angiotensin Receptor Antagonists↗
PubMed1993

[Arterial hypertension and hypokalemia].

The occurrence of hypokalemia in association with high blood pressure is suggestive of primary hypermineralocorticism since in this case both abnormalities might result from a single mechanism. However, adrenal adenomas is well as the various forms of adrenal hyperplasia appear to be quite uncommon, whereas a number of other causes of potassium depletion are far more prevalent and may be associated with essential hypertension. The demonstration of the precise mechanism of both decreased serum potassium and increased blood pressure is a prerequisite for a successful treatment.

Antihypertensive Agents↗
PubMed1993

Effect of monoclonal anti-ANP antibodies on the acute functional adaptation to unilateral nephrectomy.

The role of endogenous atrial natriuretic peptide (ANP) in the immediate response of sodium excretion to unilateral nephrectomy (UNX) was investigated in anesthetized euvolemic rats through measurement of UNX-induced change in plasma ANP concentration and the response of the remaining kidney to UNX following administration of monoclonal anti-ANP antibodies. The circulating ANP levels almost tripled (from 23 +/- 4 to 66 +/- 13 fmol/ml, P < 0.01) within two minutes after UNX, whereas no change resulted from sham intervention. In the control group receiving vehicle injection, UNX resulted in a twofold increase in urinary sodium excretion (from 1.39 +/- 0.25 to 2.88 +/- 0.28 mumol/min, P < 0.01) related to a decrease in the fractional reabsorption of sodium at both proximal and distal sites (estimated from fractional excretion of lithium). Urinary excretion of cyclic guanosine 3'-5'-monophosphate (cGMP) increased as well, but glomerular filtration rate did not change. In addition, UNX was associated with a short-lived (< 20 min) rise in systemic arterial pressure and a transient fall in right atrial pressure. Administration of monoclonal anti-ANP antibodies totally prevented the UNX-associated natriuresis by blunting both proximal and distal tubular reabsorption of sodium, and suppressed the rise in urinary cGMP excretion following UNX. The duration of the post-UNX increase in arterial pressure was longer when compared to values observed in controls. These observations indicate that ANP release is stimulated after uninephrectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1993

Converting-enzyme inhibitor versus calcium antagonist in cyclosporine-treated renal transplants.

The influence of antihypertensive treatment on the long-term evolution of arterial pressure and renal function was studied in a prospective controlled trial conducted in renal transplant recipients treated by cyclosporine. Within six months after transplantation, patients were randomly allocated to treatment by the angiotensin-converting enzyme inhibitor, lisinopril (ACEI, alone or associated with frusemide; N = 14), or the calcium antagonist, nifedipine (CA, alone or associated with atenolol; N = 11). Glomerular filtration rate (TcDTPA clearance) and effective renal plasma flow (hippuran clearance) as well as 24-hour urinary excretion of electrolytes and albumin were estimated at about 1 and 2.5 years of follow-up. Before initiation of antihypertensive therapy, the two groups were similar with regards to mean arterial pressure (119 +/- 2 vs. 120 +/- 4 mm Hg), effective renal plasma flow (285 +/- 26 vs. 248 +/- 33 ml/min/1.73 m2) and glomerular filtration rate (59 +/- 4 vs. 61 +/- 8 ml/min/1.73 m2 in the ACEI and CA groups, respectively). Both ACEI and CA treatments were associated with no change in renal function, a similar change in mean arterial pressure (ACEI -18 +/- 3; CA -13 +/- 5 mm Hg) and identical trough blood levels of cyclosporine. Urinary albumin excretion did not change significantly in any groups. Of interest, only in the ACEI group did filtration fraction significantly decrease (from 0.22 +/- 0.01% to 0.19 +/- 0.01% at final studies). These results indicate that in cyclosporine-treated transplant recipients, a satisfactory control of hypertension is obtained by chronic ACEI, which is as effective on arterial pressure as a combination of CA and atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Tubular site of the natriuresis after unilateral nephrectomy in the rat.

Unilateral nephrectomy (UNX) is followed by a prompt increase in sodium excretion from the remaining kidney. Recently, an important role for atrial natriuretic peptide (ANP) in mediating the UNX-associated natriuresis has been suggested. The present studies were undertaken to gain insight into the intrarenal mechanisms participating in the post-UNX natriuresis in circumstances in which the release or the action of endogenous ANP were suppressed by prior removal of the right atrial appendage and by administration of monoclonal anti-ANP antibodies, respectively. In anesthetized euvolemic untreated rats, UNX resulted in a twofold increase in urinary excretion of sodium (from 0.93 +/- 0.23 to 2.14 +/- 0.34 microE/min; p < 0.03), whereas glomerular filtration rate did not change significantly. Fractional excretion of lithium, an index of proximal tubular handling of sodium, increased from 30.7 +/- 3.4% to 39.4 +/- 4.0%, and fractional distal reabsorption of sodium decreased from 98.6 +/- 0.2% to 96.5% +/- 0.4% (both p < 0.006). Neither sham atrial appendectomy nor the administration of nonspecific antibodies affect the natriuretic response of the remaining kidney. The natriuretic response to UNX was abolished in right atrial appendectomized rats, as well as in rats receiving anti-ANP antibodies. Post-UNX changes in both proximal and distal tubular reabsorption of sodium were also suppressed in these animals. These observations indicate that ANP may be an important mediator of the natriuretic response to UNX and that the proximal and the distal part of the nephron contribute to the postnephrectomy natriuresis.

Animals↗
PubMed1993

Endogenous angiotensin II but not atrial natriuretic peptide modulates the effect of nicardipine on extracellular fluid partition in the rat.

OBJECTIVE: Both atrial natriuretic peptide (ANP) and the dihydropyridine derivative nicardipine lower arterial pressure and induce a shift of plasma fluid from the vascular towards the interstitial compartment. Because some calcium antagonists increase the plasma concentration of ANP, and the effect of ANP on transcapillary fluid shift requires the presence of angiotensin II, we examined the consequences of blocking the ANP and renin-angiotensin systems on the hypotensive and haemoconcentrating effects of nicardipine. METHODS: We evaluated the effects of 45-min 0.1 or 1 micrograms/kg per min nicardipine infusion on arterial pressure and haematocrit in anaesthetized, acutely binephrectomized Sprague-Dawley rats. RESULTS: Infusion of nicardipine resulted in a dose-dependent decrease in arterial pressure. Haematocrit increased by an amount corresponding to the decrease in plasma volume calculated for the relevant dose. In the presence of monoclonal anti-ANP antibodies the nicardipine-induced changes in haematocrit and arterial pressure were not affected. In rats pretreated for 2 weeks with the angiotensin converting enzyme inhibitor enalapril, as well as in rats receiving the angiotensin II receptor antagonist losartan acutely, the nicardipine-induced increase in haematocrit was abolished. In enalapril-treated rats the increase in haematocrit was entirely restored when angiotensin II was infused at a subpressor dose. The nicardipine-induced decrease in arterial pressure was not affected by pharmacological blockade of the renin-angiotensin system. CONCLUSIONS: These results demonstrate that the transcapillary shift of fluid induced by nicardipine is independent of ANP and requires the presence of a functional renin-angiotensin system, whereas its hypotensive action is independent of both ANP and angiotensin II.

Angiotensin II↗
PubMed1993

Endogenous angiotensin II modulates the effect of atrial natriuretic peptide on extracellular fluid partition.

Atrial natriuretic peptide (ANP) has been shown to promote a fluid shift from the intravascular toward the interstitial compartment and to interact with the renin-angiotensin system at the renal as well as the extrarenal level. In the present studies, the interaction between the renin-angiotensin system and the effects of ANP infusion (100 ng.kg-1 x min-1 for 45 min) on arterial pressure and hematocrit were assessed in bilaterally nephrectomized, anesthetized rats. In a first series of experiments, suppression of angiotensin II generation was achieved by chronic (10 days) treatment by the angiotensin-converting-enzyme inhibitor (ACEI) captopril in rats maintained on a low-sodium diet. ACEI pretreatment prevented the rise in hematocrit associated with ANP infusion (+2.1 +/- 0.1 vs. +5.8 +/- 0.2%, P < 0.05), without influencing the effect of ANP on arterial pressure. In ACEI-pretreated rats, acute administration of angiotensin II at a subpressor dose (2.5 ng.kg-1 x min-1) restored the ANP-induced increase in hematocrit. In a second series of experiments, acute blockade of the renin-angiotensin system was obtained by the ACEI enalaprilat or the nonpeptide angiotensin II receptor antagonist losartan (both 1 mg/kg i.v. bolus). In the presence of either enalaprilat or losartan, the ANP-induced increase in hematocrit was similarly prevented. These results indicate that the effect of ANP on vascular permeability is modulated by endogenous angiotensin II, possibly due to distinct influences of the two peptides at the level of pre- and postcapillary resistances.

Angiotensin II↗
PubMed1993

Renal and systemic adaptation to sodium restriction in aging rats.

The influence of age on the systemic and renal adaptation to dietary sodium restriction was assessed in 10-, 20-, and 30-mo-old female WAG/Rij rats. In control conditions, mean arterial pressure (MAP) was similar in all rats and plasma renin activity (PRA) was lower in 30- than in 10- and 20-mo-old rats (2.5 +/- 0.6, 5.1 +/- 0.4, and 3.9 +/- 1.0 ng ANG I.ml-1.h-1, respectively). Dietary sodium restriction was associated with a reduction in MAP in 30-mo-old rats, whereas no change occurred in 10- and 20-mo-old rats. Impairment in the early (days 1-6) renal adaptation to salt restriction was observed in 30- compared with 10- and 20-mo-old rats (6-day cumulative sodium excretion of 728 +/- 139, 437 +/- 53, and 478 +/- 37 mumol, respectively). During the 7- to 12-day period, MAP stabilized in the oldest rats and cumulative sodium excretion became similar to that of other age groups. The early increase in PRA and urinary aldosterone excretion observed in 10- and 20-mo-old rats was consistently blunted in 30-mo-old rats. These findings suggest that the delayed response of the renin-angiotensin-aldosterone system has a major role in the impaired renal and systemic adaptation to dietary sodium removal in senescent rats.

Aging↗
PubMed1993

Comparative renal and cardiac effects of tertatolol and enalapril in essential hypertension.

The influence of a 3-month antihypertensive treatment on cardiac structure and renal function was assessed in patients with uncomplicated essential hypertension randomly allocated to treatment by the nonselective beta-blocker tertatolol or the angiotensin-converting enzyme inhibitor enalapril. Both tertatolol and enalapril treatments were associated with a similar decrease in mean arterial pressure (-26 +/- 6 and -15 +/- 2 mm Hg, respectively, both p < 0.05 in comparison with baseline values) and left ventricular mass (echocardiography: -48 +/- 17 vs. -18 +/- 6 g) but no change in glomerular filtration rate (DTPA clearance). Renal vascular resistance decreased similarly in both groups. Urinary albumin excretion was not significantly modified in either group. These results indicate that a consistent reduction in arterial pressure by either treatment was associated with a proportional change in left ventricular geometry and no alteration in renal function.

Adrenergic beta-Antagonists↗
PubMed1993

Sodium and angiotensin in hypertension induced by long-term nitric oxide blockade.

The influence of dietary sodium restriction and angiotensin II blockade on hypertension induced by a 25-day period of administration of the inhibitor of nitric oxide synthesis NG-nitro-L-arginine-methyl ester (10 mg/kg twice daily by gavage) was assessed in Wistar rats fed a normal or low sodium diet. In addition, the angiotensin II receptor blocker losartan (30 mg/kg once daily by gavage) was administered before and during NG-nitro-L-arginine-methyl ester in rats fed the normal sodium diet. At the end of the studies, conscious systolic arterial pressure increased similarly in NG-nitro-L-arginine-methyl ester-treated groups maintained on normal or low sodium intake. Moreover, a 25% reduction in cardiac output due to a decrease in stroke volume was observed in both groups. A slight but significant cardiac hypertrophic response was observed in hypertensive rats irrespective of sodium intake. At the completion of studies, plasma renin activity was similar to corresponding controls in the hypertensive groups on normal or low sodium intake. Losartan totally prevented the development of hypertension as well as the decrease in stroke volume and cardiac hypertrophy associated with NG-nitro-L-arginine-methyl ester treatment in rats on normal sodium intake. In conclusion, hypertension resulting from long-term blockade of nitric oxide synthesis was not affected by dietary sodium restriction. A crucial role for the renin-angiotensin system was demonstrated in this new model of hypertension.

Angiotensin II↗
PubMed1993

Effects of calcium antagonists on adrenaline-induced hypokalaemia.

Long term treatment with nifedipine and nitrendipine, but not verapamil and diltiazem, may reduce plasma potassium levels in hypertensive patients. To test the hypothesis that this effect is related to adrenaline-mediated influx of potassium from the extracellular space, the effect of adrenaline infusions (12.5, 25 and 50 ng/kg/min) on plasma potassium levels was assessed in normotensive subjects after administration of placebo for 4 days, and after administration of nitrendipine, verapamil or diltiazem for 4 days. The adrenaline-induced decrease in plasma potassium levels was enhanced in subjects receiving nitrendipine, but was unaffected in those subjects receiving verapamil or diltiazem. The effects of adrenaline on blood glucose levels, heart rate and blood pressure were uninfluenced in subjects receiving nitrendipine or verapamil, and were blunted in subjects receiving diltiazem. These results suggest that enhancement of the adrenaline-induced intracellular transfer of potassium from the extracellular space is relatively specific to dihydropyridine calcium antagonists.

Adult↗
PubMed1993

Microalbuminuria in essential hypertension.

The prevalence and significance of microalbuminuria is not well elucidated in patients with essential hypertension. In newly detected hypertension, its prevalence ranges between 23 and 37% and albuminuria is usually well correlated with the level of arterial pressure. Interestingly, albuminuria is enhanced in overweight hypertensive patients. Antihypertensive treatment has variable influence on albuminuria, and converting enzyme inhibitors, in contrast to other agents, tend to partially correct this abnormality. Whether microalbuminuria represents a predictor of the future development of nephrosclerosis and ultimately renal failure, or a predictor of cardiovascular morbidity deserves to be investigated.

Albuminuria↗
PubMed1993

[Sodium intake and angiotensin in hypertension induced by chronic NO synthase inhibition in the rat].

The influence of dietary sodium restriction and angiotensin II blockade on hypertension induced by a 25-day period of administration of the inhibitor of nitric oxide synthesis NG-nitro-L-arginine methyl ester (L-NAME: 10 mg/kg twice daily by gavage) was assessed in Wistar rats fed a normal or low sodium diet. In addition, the angiotension II receptor blocker, losartan (30 mg/kg once daily by gavage) was administered prior to and during L-NAME in rats fed the normal sodium diet. Results expressed as mean +/- ESM are presented in the following table: [table: see text] At the end of studies, conscious systolic arterial pressure increased similarly in L-NAME-treated groups maintained on NS or LS intake. Moreover, a 25% reduction in cardiac output due to a decrease in stroke volume was observed in both groups. A slight but significant cardiac hypertrophic response was observed in hypertensive rats irrespective of sodium intake. Losartan totally prevented the development of hypertension as well as the decrease in cardiac output and the cardiac hypertrophy associated with L-NAME treatment in rats on normal sodium intake. In conclusion, hypertension resulting from chronic blockade of nitric oxide synthesis was not affected by dietary sodium restriction. A crucial role for the renin-angiotensin system was demonstrated in this new model of hypertension.

Amino Acid Oxidoreductases↗
PubMed1993

[Patterns of left ventricular adaptation to arterial hypertension].

The level of arterial pressure is not the sole determinant of cardiac adaptation to hypertension. In order to identify other factors (such as preload as well as neuro-humoral factors) we categorized by M-mode echocardiography, 192 never treated patients with mild to moderate hypertension of short duration, according to values of end-diastolic relative wall thickness (RWT) and left ventricular mass index (LVMI). Mitral regurgitation was excluded in all patients by Doppler echocardiography. Among hypertensive patients, LVMI and RWT were normal in 43% (group 1), whereas 20% had increase RWT with normal LVMI "concentric remodeling" (group 2), 24% had concentric hypertrophy (increase both LVMI and RWT) (group 3) and 13% had increased LVMI with normal RWT (eccentric hypertrophy) (group 4). Results presented as means +/- SD. [table: see text] In addition the acute response after ACE-inhibition (captopril 50 mg) of mean arterial pressure was significantly attenuated in group 4 when compared with group 1. These results suggest that the effect of arterial pressure on the heart may be modulated by volume overload (low PRA and high CI) in hypertensive patients with eccentric LV hypertrophy with normal LV function.

Adaptation, Physiological↗
PubMed1993

[Role of dietary sodium in experimental renovascular hypertension].

In order to assess the role of dietary sodium with or without chloride on the development of 2 kidney, 1 clip renovascular hypertension, 49 male Sprague-Dawley rats were fed 3 different diets for 4 weeks after clipping: ad libitum sodium chloride, sodium citrate or sodium-free diet. Sham operated rats were used as control. The final conscious systolic arterial pressure was similar in all hypertensive groups regardless of diet. No change in cardiac index occurred in clipped animals whereas total peripheral resistance raised to a similar extent. In conclusion, sodium restriction did not prevent hypertension. In addition, the anion linked to sodium had no influence on the level of arterial pressure.

Animals↗