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Biomedical subjects

J Ribstein

Publications and source records attributed to J Ribstein.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1988

Renal ornithine decarboxylase activity, polyamines, and compensatory renal hypertrophy in the rat.

We determined the role of ornithine decarboxylase (ODC) in compensatory renal hypertrophy (CRH) by relating renal ODC activity and polyamine content to kidney size, expressed as a percent of body weight, 1 wk after unilateral nephrectomy (UN). In normal rats, renal ODC activity increased from 11.0 +/- 7.4 (SD) to 36.7 +/- 15.4 pmol 14CO2.min-1.g wet wt-1 3 h after UN (P less than 0.002); 1 wk later the remaining kidney weight had increased from 0.38 to 0.46% body weight (P less than 0.001). Renal concentration of putrescine, the product of ODC's decarboxylation of ornithine, was increased 3, 8, and 48 h after UN, but concentrations of polyamines synthesized later in the pathway, spermidine and spermine, were not appreciably affected. Pretreatment with difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, as a 1% drinking water solution inhibited both base-line renal ODC activity and putrescine concentration as well as increases stimulated by UN, although concentrations of spermidine and spermine were not decreased. In these rats, CRH still occurred, since kidney weight increased from 0.36 to 0.46% (P less than 0.001). A 2% DFMO solution caused depletion of all three polyamines, but CRH took place nevertheless. In hypophysectomized rats, both increased renal ODC activity and CRH occurred as well, indicating that these two consequences of UN do not require intact pituitary function. Although increased renal ODC activity and CRH after UN are correlated in normal and hypophysectomized rats, CRH takes place in rats treated with DFMO despite inhibition of ODC activity and depletion of polyamines.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Response of atrial natriuretic peptide to acute saline loading in essential hypertension.

To further investigate the mechanism(s) of the exaggerated natriuretic response of hypertensives to volume expansion (VE; 1,800 ml iv isotonic saline over 3 h), the plasma levels of immunoreactive atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (HT). NT and HT groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in HT, mean +/- SE). In response to VE, ANP increased to the same extent in both groups (a change of 19.3 +/- 5.2 in NT and of 22.2 +/- 7.1 pg/ml in HT) despite the finding of an exaggerated natriuretic response to VE in essential hypertension (36 +/- 3.5 in NT and 54.9 +/- 6.3 nmol/3 h in HT, P less than 0.02). In addition, the fall in hematocrit and serum protein associated with saline infusion was less marked in HT than NT. The change in ANP induced by VE was inversely correlated with the percent fall in hematocrit and the increment in the fractional excretion of sodium in both groups. These observations suggest that ANPs may participate in the control of the renal response to isotonic VE; however they do not support an unequivocal influence of ANP in the exaggerated natriuretic response to VE of patients with essential hypertension.

Adult↗
PubMed1988

Effect of preoperative renin-angiotensin system blockade on hypertension following coronary surgery.

Renin-angiotensin system activation is suspected of being involved in postcoronary surgery hypertension, but appears to be useful in maintaining blood pressure during anesthesia and cardiopulmonary bypass. To clarify these points, 19 patients were compared: ten as a control group and nine who received captopril during two days before surgery. Anesthesia was the same for the two groups, and cardiopulmonary bypass ensured nonpulsatile flow rates. Anesthesia induced a slight decrease in the mean arterial blood pressure of the treated group (91.1 +/- 3.3 mm Hg to 83.3 +/- 3.9 mm Hg), which did not occur in the control group (89.9 +/- 5.8 mm Hg to 89.7 +/- 4.9 mm Hg). During cardiopulmonary bypass, the mean arterial blood pressure was maintained at comparable levels in the two groups (65.6 +/- 3.5 mm Hg in the control group, 72.6 +/- 3.0 mm Hg in the treated group), with same pump flow rates. After cardiopulmonary bypass, the mean arterial blood pressure returned nearly to prebypass values. Postoperatively, three patients in the control group and four in the treated group developed hypertension. Thus, preoperative renin-angiotensin system blockade by a converting-enzyme inhibitor did not impair blood pressure regulation during anesthesia and cardiopulmonary bypass, but failed to prevent hypertension following coronary surgery.

Captopril↗
PubMed1988

[Role of atrial natriuretic peptide in the renal response to acute volume expansion in the normal and essential hypertensive patient].

An exaggerated natriuretic response to volume expansion (VE) is observed in many essential hypertensive patients. The plasma levels of atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (EH) during VE (1 800 ml isotonic saline IV over 3 hours). NT and EH groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in EH, mean +/- sem). In response to VE, ANP increased to the same extent in both groups (a change of + 19.3 +/- 5.2 in NT and 22.2 +/- 7.1 pg/ml in EH) despite the marked difference in observed natriuresis (36 +/- 3.5 in NT and 54.9 +/- 6.3 mmol/3 in EH, p less than 0.02). The change in ANP induced by VE was inversely correlated with the fall in hematocrit and the variation in fractional excretion of sodium in both groups. These results suggest that atrial natriuretic peptide may participate in the control of the renal response to isotonic volume expansion, but they do not support a predominant role of atrial natriuretic peptide in the exaggerated natriuretic responses to volume expansion of patients with essential hypertension.

Adult↗
PubMed1988

Comparative effect of captopril and nifedipine in normotensive patients with incipient diabetic nephropathy.

The effect of a six-week treatment by placebo, the calcium channel blocker nifedipine or the converting enzyme inhibitor captopril was assessed in normotensive patients with insulin-dependent diabetes and incipient nephropathy. In response to captopril and nifedipine, arterial pressure decreased slightly and to a similar extent. These drugs resulted in opposite effects on urinary albumin excretion (increase in urinary albumin excretion by 40% during nifedipine and decrease by 40% during captopril treatment). No change in urinary albumin excretion was observed in the placebo group. This observation of opposite changes in urinary albumin excretion in the presence of a similar fall in arterial pressure suggests that the effect of captopril and nifedipine on urinary albumin excretion results from some difference in their intrarenal action.

Adult↗
PubMed1988

[Malignant arterial hypertension disclosing late congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency].

17 alpha-hydroxylase deficiency is a rare form of congenital abnormality in steroid synthesis, usually associated with moderate arterial hypertension and suppression of the renin-angiotensin system in a young adult. We report on a 45 years old woman with malignant hypertension (220/135 mmHg, severe retinopathy with papilledema, progressive renal insufficiency with serum creatinine over 300 mumol/l) of recent onset. Biological exploration revealed a metabolic alkalosis, a moderate hypokalemia (3 mmol/l), with elevated urinary excretion of potassium. Plasma aldosterone concentration (33 ng/dl) and plasma renin activity (17 ng/ml/h) were elevated. Acute captopril administration was followed by a marked (-29 p. 100) decrease in mean arterial pressure. In this 46 XX patient, a primary amenorrhea had never been explored; clinical examination disclosed the absence of female secondary sex characteristics. Plasma cortisol was low (203 mmol/l) as were plasma androgens (testosterone 0.55, androstene dione 0.19, delta HEA less than 0.1 nmol/l respectively) and oestrogens (oestradiol 59 nmol/l). Elevated levels of progesterone and pregnenolone sulfate (12.1 and 2027 nmol/l respectively) contrasted with decreased levels of 17 OH progesterone (0.35 nmol/l). Computed tomography revealed a subnormal right adrenal gland and a pseudo-tumoral aspect on the left side. Treatment with dexamethasone and combined antihypertensive drugs (captopril, nifedipine and atenolol) resulted in normalisation of blood pressure and secretion of renin and aldosterone but renal function did not fully recovered. Thus, the hypertension of 17 alpha-hydroxylase deficiency can follow a malignant course in association with a marked activation of the renin-angiotensin system.

Adrenal Hyperplasia, Congenital↗
PubMed1987

[The hypokalemic effect of adrenaline is increased by nitrendipine in normal man].

Calcium blockers of the dihydropyridine group may affect serum potassium level through an influence on the epinephrine mediated fall in serum K+. The effect of epinephrine infusion (12.5, 25 and 50 ng/kg/min) was assessed during placebo and after a 4-day treatment by nitrendipine in normal man. Nitrendipine treatment was associated with an enhancement in the fall of serum potassium induced by epinephrine. By contrast the response of arterial pressure, heart rate as well as the increase in blood glucose, plasma renin activity and the fall in plasma aldosterone and serum insulin levels induced by epinephrine were not affected by nitrendipine. Nitrendipine may potentiate the Na, K-ATPase stimulatory effect of epinephrine. Serum potassium should be carefully monitored in clinical situations associated with a consistent increase in circulating levels of epinephrine.

Adult↗
PubMed1987

[Determinant factors in the acute functional deterioration caused by the inhibition of the conversion enzyme in reno-vascular arterial hypertension].

Deterioration of renal function may be elicited by converting enzyme inhibition (CEI) in patients with bilateral (BI) or solitary kidney (SK) renal artery stenosis, but the determinants of this complication are not clearly delimited. The effect of acute administration of captopril on arterial pressure, glomerular filtration rate (GFR) and effective renal plasma flow was assessed in 10 BI and 10 SK hypertensive patients with a mean GFR of 64 +/- 5 ml/min. CEI induced a decrease in MAP of 8 +/- 2 p. 100 and a fall in GFR of 25 +/- 8 p. 100; GFR fell by more than 20 p. 100 in 5/10 BI and 8/10 SK. Filtration fraction (FF) decreased by 16 +/- 5 p. 100. CEI-induced change in GFR was not related to the change in MAP, but was inversely correlated with pre-C FF; GFR always fell when FF was higher than 0.28. Surgical correction of the stenosis suppressed the C-induced decrease in GFR in 5 SK patients in whom it initially fell. In conclusion, basal FF, a probable index of intrarenal angiotensin II activity, rather than a fall in systemic blood pressure, is the main predictor of acute deterioration of renal function after converting enzyme inhibition.

Adult↗
PubMed1986

Effect of nifedipine in hypertension not controlled by converting enzyme inhibitor and 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 blood pressure, 172 +/- 6/111 +/- 4 mmHg) by the association of a converting enzyme inhibitor and a diuretic. Nifedipine administration induced a marked decrease in blood pressure (to 133 +/- 3/85 +/- 3 mmHg), serum potassium and plasma aldosterone. Following adequate control of hypertension and because of severe hypokalaemia in some patients, the diuretic was discontinued in 10 subjects. After 1.7 +/- 0.5 months of treatment by the converting enzyme inhibitor and nifedipine, no change in arterial pressure occurred whilst serum potassium returned to normal in most patients. These results demonstrate that nifedipine may be useful in patients with residual elevation of arterial pressure when treated by converting enzyme inhibitor and diuretic. However, in such patients serum potassium level 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↗
PubMed1986

Acute renal effects of captopril in patients with congestive heart failure.

The effect of acute administration of the angiotensin-converting enzyme inhibitor captopril on arterial pressure, glomerular filtration rate, and renal plasma flow was assessed in 16 patients with severe congestive heart failure. Following administration of captopril, mean arterial pressure (MAP) fell in all cases, whereas effective renal plasma flow increased from 27% to 88% in 10 patients, remained unchanged in 4, and decreased by 60% and 93% in 2 patients in whom MAP fell to 54 and 47 mmHg, respectively. Effective renal plasma flow and glomerular filtration rate values achieved after captopril were both positively correlated with postcaptopril MAP. The results of this study suggest that the renin-angiotensin system plays a major role in the regulation of MAP and the renal vasoconstriction associated with severe congestive heart failure. However, angiotensin blockade may induce a deterioration in renal function in patients in whom arterial pressure falls to markedly low values, thus suggesting an influence in angiotensin in renal autoregulation in these patients.

Adult↗
PubMed1986

[Urinary excretion of kallikrein and sensitivity of blood pressure to acute sodium loading in healthy subjects].

Acute extracellular volume expansion (VE) by isotonic saline is associated with variable change in mean arterial pressure (MAP) in normotensive subjects (NT). Following VE by 1,800 ml isotonic saline in 3 h, two patterns of MAP response were observed in NT: either an increase by more than 10% (SS: sodium or VE sensitive, n = 12) or no change (NSS: non-sodium or VE sensitive, n = 14). We assessed in all subjects the response to VE of glomerular filtration rate (GFR), urinary sodium (UNaV) and kallikrein (UKalV) excretion rate, plasma renin activity (PRA) and aldosterone concentration (PAC). Family history of blood pressure was not different between the groups. In response to VE, MAP increased (88 +/- 3 to 102 +/- 4 mmHg) in group SS and did not change in group NSS (83 +/- 3 to 85 +/- 3 mmHg). Whilst UNaV measured during the hour prior to VE was similar in both groups, the total amount of sodium excreted during VE was higher in group SS than in group NSS (52 +/- 9 vs 32 +/- 3 mmol/3 h, p less than 0.05). Control GFR as well as changes in GFR associated with VE were similar in both groups. A similar decrease in PRA and PAC was observed in both groups and pre-VE values were identical. UKalV was lower in SS than NSS subjects during the pre-VE control jour (0.42 +/- 0.09 vs 0.74 nKat/h; p less than 0.05) and during VE (1.14 +/- 0.16 vs 2.5 vs 0.47 nKat/3 h; p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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↗