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Biomedical subjects

A Mimran

Publications and source records attributed to A Mimran.

At least 163 records · Page 9Linked to original sources
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

Systemic and regional haemodynamic profile of diuretics and alpha- and beta-blockers. A review comparing acute and chronic effects.

The influence of the acute and chronic administration of antihypertensive agents on blood flow to various organs which are known targets of hypertension is important in the determination of drug therapy for this disorder. In association with the frequently observed fall in cardiac output and increase in total peripheral resistance in response to acute administration, beta-blockers may induce a decrease in blood flow to the brain and kidney. However, during chronic treatment it has been widely shown that total peripheral resistance returns to pretreatment levels (except for labetalol, a beta-blocker with alpha-blocking properties) whilst renal and cerebral blood flows are unaffected. Although alpha-blockers acutely lower blood pressure and induce a baroreflex-mediated increase in heart rate and cardiac output while not affecting cerebral blood flow, during chronic treatment no change in systemic or cerebral or renal blood flow is observed. Diuretics and dietary sodium restriction, which are the most widely used therapeutic interventions, are usually well tolerated; however, in aged patients in whom renal adaptation to sodium depletion is impaired, deterioration of renal function may be observed.

Adrenergic alpha-Antagonists↗
PubMed1988

Enhanced urinary kallikrein excretion in response to a moderate sodium load in genetically hypertensive rats.

Experiments were performed to compare the diuretic and natriuretic response to a moderate saline load between 12-week-old conscious spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) male rats. The animals were infused intravenously with 0.9% NaCl, first for a 1-h equilibration period, at a rate of 20 microliters/min, then for a 2-h salt-loading phase at 40 microliters/min, and finally during a 1-h recovery at 20 microliters/min. Cumulative renal excretion of water and sodium was similar in SHR and WKY rats. In contrast, urinary kallikrein excretion (amidolytic assay) during the saline-expansion and recovery phases was significantly higher in SHR than in WKY rats. At the end of the salt-loading phase, plasma levels of atrial natriuretic peptide (ANP) were higher in SHR than in WKY rats (p less than 0.05). This was also true in animals infused with 5% dextrose instead of 0.9% NaCl. Splanchnic nerve activity remained stable throughout the study in SHR as well as in WKY rats. These data therefore indicate that SHR excrete water and sodium similarly to WKY rats when they are subjected to a moderate sodium load. Neither ANP nor the sympathetic nervous system seems to be directly implicated in the renal response to the moderate saline expansion. Whether the enhanced urinary kallikrein excretion observed in SHR reflects an active participation of the renal kallikrein-kinin system in their sodium handling remains uncertain.

Animals↗
PubMed1988

Effect of perindopril on the renal haemodynamic changes associated with adaptation to sodium restriction in the rat.

We assessed the effect of increasing doses of perindopril on the renal adaptation to withdrawal of dietary sodium in rats. In treated animals, the amount of sodium lost during the 6-day observation period was higher than that found in untreated rats, but only at doses that significantly inhibited the circulating angiotensin converting enzyme (ACE). Sodium loss was not enhanced by increasing the dose of the agent. In contrast, the renal vasodilatory effect of perindopril was dose-dependent, and was significant with the lowest perindopril dose, which did not impair sodium conservation. These results suggest that in the rat, perindopril may act on the renal vasculature before impairing the natriuretic adaptation in response to sodium restriction.

Adaptation, Physiological↗
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↗
PubMed1987

Vasoconstrictor role for vasopressin in conscious, sodium-depleted rats.

To define the role of vasopressin as a vasoconstrictor hormone in sodium depletion, systemic hemodynamics and regional blood flow distribution were examined in conscious Sprague-Dawley rats after 6 days of a low-sodium diet. Studies were performed after selective or combined blockade with the vasopressin antagonist [d(CH2)5Tyr(Me)]AVP (AVPA), enalaprilat (CEI), and phentolamine (PHENTOL). Plasma levels of vasopressin were increased significantly after CEI and increased further after PHENTOL and CEI plus PHENTOL. AVPA had no effect on blood pressure, whether given alone or in the presence of PHENTOL, CEI, or CEI plus PHENTOL. Significant falls in peripheral vascular resistance associated with reflex increases in cardiac output were observed when AVPA was given to animals pretreated with either CEI or PHENTOL but not both. AVPA alone produced no significant changes in regional blood flow distribution, but a vasoconstrictor action of vasopressin in the renal vascular bed was revealed after prior treatment with CEI or PHENTOL. Muscle blood flow was also increased in the PHENTOL plus AVPA group compared with the PHENTOL group. No significant additional effects of AVPA were revealed by pretreatment with CEI, PHENTOL, or CEI plus PHENTOL for mesenteric, hepatic, splenic, or cerebral vascular beds. It is suggested that vasopressin acts as a vasoconstrictor hormone in conscious sodium-depleted rats when either the renin-angiotensin system or alpha-adrenergic system is inhibited but not when both systems are blocked. The renal vascular bed is an important site for vasopressin-induced vasoconstriction under these circumstances.

Adaptation, Physiological↗
PubMed1987

Ketanserin versus nifedipine in the treatment of essential hypertension in patients over 50 years old: an international multicenter study.

The serotonergic antagonist ketanserin (K) was compared to nifedipine (N) in a five-center international study on hypertensive patients over the age of 50 years. After a 4-week placebo run-in period, patients were randomly assigned to receive for 3 months either ketanserin (40 mg b.i.d. after 2 weeks of 20 mg b.i.d.) or nifedipine (20 mg N retard b.i.d.). After 1 month, monotherapy patients whose blood pressure was not sufficiently reduced received a diuretic in combination therapy. At the end of the active treatment period, patients who had remained on monotherapy received placebo until hypertension returned or for a maximum of 2 months. One hundred and seventeen patients were entered in the study, 58 on K and 59 on N. More patients switched to combination with a diuretic in the K group (14 patients) than in the N group (6 patients). The overall reduction in blood pressure was similar for K and N. Total response rate was high (96%) for the two drugs. Blood pressure was reduced both at peak and trough drug levels. No orthostatic reactions were observed, and no rebound hypertension occurred at discontinuation of therapy. Ketanserin monotherapy slightly decreased heart rate (-1 beats/min). whereas N produced a significant increase (+6 beats/min). Body weight significantly increased with K (+1.1 kg) and was unchanged with N. More patients complained of adverse reactions during N monotherapy (47%) than during K monotherapy (34%). Flushing and leg edema were more frequent with N.

Blood Pressure↗
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

Double-blind comparison of the cardioselective beta-blockers bisoprolol and atenolol in hypertension: the Bisoprolol International Multicenter Study (BIMS).

The antihypertensive efficacy and tolerability of bisoprolol and atenolol were compared in the Bisoprolol International Multicenter Study (BIMS). In 104 patients with essential hypertension (21 to 70 years of age and diastolic blood pressures (DBP) of 100-120 mm Hg in the sitting position), after a four-week placebo period, the active drug was given in a random double-blind crossover design (10 to 20 mg bisoprolol, 50 to 100 mg atenolol) for eight weeks each, with a 2 to 6 week placebo wash-out phase between active therapy. All blood pressures were recorded 24 h after drug intake. Of the 104 patients, 10 were withdrawn during the study because of unwanted effects, unsatisfactory blood pressure response, or intercurrent disease, leaving 94 for intraindividual comparisons. After 8 weeks active treatment with individually titrated dose, there were slightly, but significantly greater falls in blood pressure with bisoprolol (p less than or equal to 0.05). Diastolic target pressures of less than or equal to 95 mm Hg were reached in 68% with bisoprolol and 56% with atenolol (p less than or equal to 0.05; Mc Nemar). There was no between treatment group difference in the patients' self-assessed well-being. For both drugs, response rates were greater in patients below the age of 60 years than in those above 60 years. Better antihypertensive responses were observed with bisoprolol in patients regularly smoking cigarettes.

Adrenergic beta-Antagonists↗
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↗