Biomedical subjects

J Ribstein

Publications and source records attributed to J Ribstein.

At least 55 records · Page 3Linked to original sources

PubMed1994

Angiotensin-converting enzyme inhibitors versus calcium antagonists in the progression of renal diseases.

In addition to factors such as protein intake or hyperlipidemia, hypertension contributes to the progressive deterioration of renal function in experimental animal models of renal disease, and has a prominent role in the imbalance of intrarenal hemodynamics. Reduction of arterial pressure was shown to alter the course of human chronic renal disease. In patients with diabetic as well as nondiabetic nephropathy, the lowering of proteinuria by angiotensin-converting enzyme inhibitors is greater than that observed with other antihypertensive drugs and appears to be independent of blood pressure control alone, whereas albuminuria may be unaffected or worsened during nifedipine treatment. Angiotensin-converting enzyme inhibitors may afford better protection than conventional treatment at various stages of diabetic nephropathy and prevent the evolution from incipient to overt nephropathy. In patients with nondiabetic renal disease, no unequivocal evidence exists for such a protective effect. In renal transplant recipients receiving cyclosporine, converting enzyme inhibitors and calcium antagonists are equally effective in the control of hypertension and both leave unaltered the glomerular filtration rate. It remains to be demonstrated, using adequate study designs, whether a particular class of agent is superior to another in patients with chronic renal disease.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1994

Is microalbuminuria a marker of early intrarenal vascular dysfunction in essential hypertension?

The relation between basal intrarenal hemodynamics and the renal response to acute inhibition of angiotensin-converting enzyme by captopril and albuminuria was assessed in 106 lean patients with essential hypertension without detectable proteinuria. It was observed that the microalbuminuric group (24.5% of the total population) was characterized by a higher systemic arterial pressure, a lower level of high-density lipoprotein cholesterol, and similar mean values of age, duration of hypertension, glomerular filtration rate, renal plasma flow, filtration fraction, and plasma renin activity when compared with normoalbuminuric subjects. In response to captopril, a significant renal vasodilatation without a change in glomerular filtration rate or a fall in filtration fraction was observed in normoalbuminuric patients only. In contrast, the renal vasodilator response was abolished in microalbuminuric subjects, together with blunting of the rise in plasma renin activity associated with captopril. This occurred despite similar indexes of activity of the endogenous renin-angiotensin system. It is suggested that microalbuminuria may be a marker of early functional or fixed intrarenal vascular dysfunction in never-treated lean patients with essential hypertension.

Adolescent↗

PubMed1994

Influence of dopamine and angiotensin II blockade on the acute response to unilateral nephrectomy in rats.

Unilateral nephrectomy (UNX) is followed by a prompt functional adaptation (as well as initiation of compensatory growth) in the contralateral kidney. We assessed the possibility that dopamine (DA) receptor antagonism and angiotensin-converting enzyme inhibition may influence the acute natriuretic response to UNX of the remaining kidney in euvolemic anesthetized Sprague-Dawley rats with or without pretreatment by haloperidol or enalapril. Twenty to 80 min after UNX, urinary excretion of sodium and potassium approximately doubled and fractional excretion of lithium (an index of proximal tubular handling of sodium) increased by about one third in untreated rats, whereas glomerular filtration rate, renal plasma flow and mean arterial pressure (MAP) did not change significantly. Haloperidol infusion blunted the post-UNX increase in fractional excretion of lithium without affecting the natriuretic/kaliuretic response of the remaining kidney. Enalapril pretreatment resulted in lower MAP and marked renal vasodilation at baseline but no significant alteration in the response to UNX. These results indicate that the magnitude of post-UNX natriuresis is not affected by suppression of angiotensin II (AII) generation or blockade of DA receptors. The lithium clearance data suggest that the immediate natriuretic response to UNX can be ascribed to both a proximal and a distal tubular phenomenon.

Angiotensin II↗

PubMed1994

[Left ventricular performance and morphologic myocardial changes in untreated hypertensive patients].

Left ventricular contractile performance and geometric adaptation to hypertension were investigated in 255 patients with untreated essential hypertension and 160 normotensive subjects by M-mode echocardiography. Because all "ejection-phase" measurements are affected by changes in afterload, ventricular performance was estimated at the operating level of systolic wall stress by the afterload-corrected fractional shortening. Mitral regurgitation was excluded in all patients by Doppler echocardiography. Patients were categorized according to values of end-diastolic relative wall thickness and left ventricular mass index. Among hypertensive patients, ventricular mass and relative wall thickness were normal in 44%, whereas 20% had increase relative wall thickness with normal ventricular mass "concentric remodeling", 22% had concentric hypertrophy (increase both ventricular mass and relative wall thickness) and 14% had increased ventricular mass with normal relative wall thickness (eccentric hypertrophy). Arterial pressure and body mass index were higher in patients with concentric hypertrophy. Left ventricular contractile performance paralleled ventricular geometry, with a decrease of the afterload-corrected fractional shortening in the group with concentric remodeling and hypertrophy, whereas systolic function was normal in the eccentric group despite higher level of systolic wall stress. This study suggests a strong dependence of left ventricular mass with chamber size and myocardial contractility. Thus arterial pressure was not the sole determinant of left ventricular hypertrophy in essential hypertension. The respective role of this factors remains to be determined.

Adaptation, Physiological↗

PubMed1994

[Should substitution criteria be used in hypertensive disease?].

A number of methods, some of which are still in the development phase, enable progressively more accurate assessment of structural and/or functional changes of the target organs of hypertension. The notion that these changes may be used as a substitution criterion in the evaluation of hypertensive disease is at the heart of the concept of preclinical cardiovascular disease: in its theoretical and practical aspects, this concept stipulates that the preclinical disease is an intermediate stage between exposure to the risk factor of hypertension and the advant of morbid or mortal cardiovascular events, and it suggests that the evaluation of the preclinical disease leads to a more accurate stratification of cardiovascular risk than measurement of the risk factors alone. However, at present, none of the parameters proposed (albuminuria, left ventricular mass, arterial wall thickness) is a validated substitution criterion; but many arguments indicate that the use of these parameters as intermediate criteria is justified under certain conditions.

Arteriosclerosis↗

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

Ambulatory monitoring of blood pressure in normal pregnancy.

The definition of hypertensive disorders in pregnancy is plagued by many difficulties, in part related to the limits of intermittent clinic readings of blood pressure. In order to better define the evolution of arterial blood pressure in normal subjects during normal pregnancy, casual and ambulatory (Spacelabs 90207, n = 22 or Diasys 200, n = 26) measurements of blood pressure were performed at gestational months 3, 6, and 9, in 48 normal women aged 18 to 39, both nulliparas (n = 19) and multiparas (n = 29). Ambulatory blood pressure levels were lowest in the first gestational trimester (24-hour mean: 104 +/- 8/63 +/- 6 mm Hg) and rose by a small increment during the last trimester (109 +/- 8/67 +/- 7 mm Hg at 8 months). Mean daytime ambulatory pressure was almost superimposable to clinic measurements at the three time points. A day-night variation in blood pressure level was detectable in all subjects at each recording. It is concluded that during normal pregnancy, ambulatory blood pressure levels were highest in the day and lowest at night at all gestational ages and increased only minimally before the ninth month. Reference values, as defined by the percentile distribution of daytime and nighttime systolic and diastolic blood pressure, may help define more precisely an alteration in the level and/or the circadian variation of arterial blood pressure during abnormal pregnancies.

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

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

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

[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

Early systemic and renal responses to nephrectomy in normotensive kidney donors.

The present studies were designed to assess the effect of uninephrectomy (UNX) on arterial pressure and renal excretory function in normal subjects. Baseline values of arterial pressure, renal function, parameters of the renin-angiotensin and renal kallikrein-kinin systems and the response to acute saline loading (VE, 1800 ml in 3 h) were estimated in 18 kidney donors prior to and 1 year following UNX. Within the follow-up period of 14 +/- 1 months mean arterial pressure (MAP) increased by 7 +/- 2 mmHg, creatinine clearance decreased by 38 +/- 4%, plasma renin activity (PRA) decreased, urinary kallikrein remained unchanged, and the renal response to VE was blunted. According to individual changes in MAP associated with UNX, subjects were classified as responders (R, increase in MAP > or = 10%, n = 8) and non-responders (NR, n = 10). Age, incidence of a family history of hypertension, decrease in creatinine clearance, and predonation PRA, urinary kallikrein, and the natriuretic response to VE were similar in the two groups. However, following UNX, PRA decreased whereas 24-h urinary sodium and thus sodium intake increased only in the R group. In conclusion, in normotensive subjects a 50% reduction in renal mass may result in a consistent increase in MAP and sometimes the development of de novo hypertension (4/18 subjects). Baseline characteristics as well as the predonation renal response to VE do not provide a means of detecting kidney donors in whom arterial pressure will increase consistently after UNX.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

[Arterial hypertension, hyperinsulinism and insulin resistance].

The incidence of hypertension is increased in obesity, a state associated with an insulin resistance syndrome. By using an euglycemic clamp method, Ferrannini et al. demonstrated the existence of an insulin resistance state in patients with essential hypertension. However, the body mass index of the subjects studied appeared to be slightly excessive. This abnormality has not been observed in patients with secondary hypertension. Insulin resistance is probably localized to peripheral tissues such as muscles and may be associated with other cellular abnormalities. Can insulin resistance, characterized by a raised circulating insulin concentration in the presence of normal blood glucose, be responsible for certain "modifications" associated with essential hypertension? Insulin induces sodium retention and increases the aldosterone-secreting effect of angiotensin II. These effects are likely to promote a rise in blood pressure and an increase in the sensitivity of vessels to endogenous substances. Moreover, insulin is a known growth factor and is involved in lipoprotein metabolism. If insulin resistance plays an important role in the maintenance of complications of essential hypertension, it is important that the treatments used tend to correct this anomaly. Thiazide diuretics and beta-blockers aggravate insulin resistance while angiotensin converting-enzyme inhibitors correct this condition.

Adult↗