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Biomedical subjects

L Favre

Publications and source records attributed to L Favre.

At least 37 records · Page 2Linked to original sources
PubMed1986

Effect of noradrenaline, vasopressin and angiotensin II on renal prostaglandins in man.

To examine the response of renal prostaglandins (PG) to systemic and renal vasoconstriction noradrenaline (NA), arginine vasopressin (AVP) and angiotensin II (ANG II) were each infused into eight healthy female subjects for 3 h on different days. Urinary excretion of PGE2, PGF2 alpha and 6-keto-PGF1 alpha was determined hourly. NA and ANG II stimulated excretion of PGF2 alpha significantly, but not of PGE2 or 6-keto-PGF1 alpha. AVP stimulated renal PGF2 alpha and 6-keto-PGF1 alpha significantly, but not PGE2. A weak correlation was found between urinary PGF2 alpha and diastolic blood pressure during NA and ANG II infusions, but not during AVP infusion. The release of renal PG does not appear to constitute an obligatory and concomitant response to the blood pressure rise induced by the pressor agonists. The greater response of PGF2 alpha than of PGE2 may result from a preferential direct effect on PGF2 alpha secretion or from an increased conversion of PGE2 into F2 alpha.

Adult↗
PubMed1986

Effects of bopindolol on renal function.

The effect of the long-acting beta-blocking agent bopindolol on renal function was assessed in 10 healthy normotensive volunteers and 10 hypertensive patients. The subjects received 1 mg bopindolol at 8 p.m. for 21 days. The following determinations were made at 8 a.m. on recumbent, fasting subjects before day 0 (D0) and 12 h after day 1 (D1) the first dose of bopindolol, and on the 21st day of treatment (D21): blood pressure (diastolic = DBP), glomerular filtration rate (GFR) and renal plasma flow (RPF) as reflected by the plasma disappearance of 51Cr-EDTA and 125I-hippuran, plasma concentrations and 2- and 24-h urinary excretion of electrolytes, creatinine, and proteins and osmolality of the urine. Plasma renin activity was assessed on standing subjects. Following bopindolol administration GFR, RPF, and filtration fraction remained stable, in spite of a fall of DBP from 80 +/- 7 to 76 +/- 4 and to 72 +/- 9 mm Hg in normotensives (p less than 0.05) and from 106 +/- 11-96 +/- 10 and to 91 +/- 8 mm Hg in hypertensives (p less than 0.05) on D1 and D21, respectively. The drops in DBP at D1 correlated weakly with the pretreatment renin levels (p = 0.074, p less than 0.05). All the other variables remained stable, including diuresis, free water clearance, and fractional sodium excretion. It is concluded that in contrast to many other anti-hypertensive drugs including several beta blockers, bopindolol does not reduce renal function during short- or medium-term treatment in normal volunteers or hypertensive patients.

Adolescent↗
PubMed1986

Effect of bopindolol on the circadian blood pressure profile in essential hypertension.

The effect of bopindolol on circadian blood pressure and heart rate profile was evaluated by means of an automatic recording technique (Pressurometer II). Blood pressure and heart rate was measured every 15 min for 24 h in 11 ambulant hypertensive patients. Recordings were made after 2 weeks on placebo then after treatment for 4 and 8 weeks with single daily doses of 0.5 or 1 mg bopindolol, according to a double-blind crossover plan. The results show a significant fall in the mean 24-h values for systolic and diastolic blood pressure and heart rate on both dosages of bopindolol. The low-dose level had a more marked effect on the day phase of the blood pressure profile, whereas the high-dose level affected day and night phases equally. Over all, the circadian rhythms of blood pressure and heart rate were not influenced. In conclusion, bopindolol has a well-defined antihypertensive effect on the various phases of the 24-h blood pressure and heart rate profiles.

Adrenergic beta-Antagonists↗
PubMed1986

Dynamic response of PG synthesis to peptide hormones and osmolality in renal tubular cells.

A superfusion technique was adapted to collagenase-dispersed renal medullary and cortical tubular cells to study prostaglandin (PG) synthesis in response to arginine vasopressin (AVP), angiotensin II (ANG II), bradykinin (BK), Ca2+ ionophore A23187, and to changes in osmolality. Medullary and cortical cells promptly responded to the stimuli by an increase in PGE2 and PGF2 alpha production, whereas 6-keto-PGF1 alpha was not detected. AVP and BK were active on medullary cells, and ANG II was active mainly on cortical cells. A23187 stimulated PG synthesis in both cells but predominantly in the medulla. PG synthesis was dependent on the presence of extracellular Ca2+. The Ca2+ entry blocking agents verapamil and lanthanum did not inhibit the PG response to AVP, BK, and ANG II. Thus peptide hormone-stimulated PG synthesis in renal tubular cells did not depend on Ca2+ influx through channels blocked by these agents. Hyperosmolar NaCl or mannitol stimulated PG synthesis in cortical and, more markedly, in medullary cells. Hyperosmolar urea inhibited PGE2 synthesis stimulated by peptide hormones, NaCl, and A23187 in both cell preparations. In conclusion, the superfusion of isolated tubular cells is a useful method to study the dynamic aspects of renal PG release in response to various sequentially applied stimuli.

Angiotensin II↗
PubMed1986

Osmolar stimulation of vasopressin secretion in man: comparison of various protocols.

The osmolar stimulation of vasopressin (AVP) release has been studied in 5 healthy subjects using two comparative protocols (infusion of 5% NaCl over 2 h vs 2.5% NaCl over 3 h). As AVP may be secreted by episodic bursts, AVP plasma concentrations were determined both in discrete plasma samples and in integrated samples drawn continuously by a pump over periods of 30 min. There was an earlier rise of plasma osmolality and AVP during the 5% NaCl infusion, but the final maximal value of plasma AVP did not differ in the two protocols. Plasma AVP rose from 1.3 +/- 0.7 to 3.8 +/- 1.5 during the 2.5% NaCl infusion and from 1.1 +/- 0.1 to 3.9 +/- 0.6 pg/ml during the 5% NaCl infusion. In both protocols a significant correlation obtained between the discrete and the integrated values of plasma AVP (r = 0.77 and r = 0.84 respectively, P less than 0.05). These results demonstrate that the two protocols of osmolar stimulation are equipotent in releasing AVP and do not induce episodic secretion.

Adult↗
PubMed1986

Calcium-channel inhibition in pheochromocytoma.

Nifedipine, a calcium-antagonist and potent vasodilator, was tested in three patients with pheochromocytoma. In two patients who were normotensive, nifedipine prevented a rise in blood pressure but not in plasma epinephrine and norepinephrine following the iv injection of the dopamine-antagonist metoclopramide. In another patient who was hypertensive, nifedipine was as effective in lowering blood pressure as labetalol or phenoxybenzamine, and did not modify the elevated plasma and urinary catecholamines. Nifedipine appears to control hypertension in pheochromocytoma, without altering catecholamine levels, suggesting that calcium-channel blockade interferes with catecholamine vascular action but not with tumoural catecholamine release. Calcium-antagonists may be helpful in preventing the pressor complications of provocative tests used in the screening of pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1986

Blood pressure regulation on low and high sodium diets in normotensive members of normotensive or hypertensive families.

In members of hypertensive families a high sodium intake may have a pressor effect. The mechanism mediating the sodium sensitivity is unclear. Blood pressure, exchangeable sodium, plasma levels of norepinephrine, epinephrine, renin and aldosterone, the pressor response to infused norepinephrine or angiotensin II and the urinary excretion of prostaglandin (PG) E2 and F2 alpha were measured after 7 days of low sodium diet (urinary sodium 13 +/- 10 s.d. mmol/24 h) and 7 days of high sodium intake (urinary sodium 268 +/- 97 mmol/24 h) in 10 normotensive men without and 13 men with family history of essential hypertension. After the low sodium phase, blood pressure, heart rate, exchangeable sodium, plasma levels of norepinephrine, epinephrine, renin and aldosterone, pressor doses of norepinephrine or angiotensin II and the urinary excretion of PGE2 or PGF2 alpha did not differ between the two groups. After the high sodium phase, blood pressure increased only in subjects with positive (P less than 0.05) but not in those with negative family history. In the two groups exchangeable sodium increased (P less than 0.05) and plasma levels of NE (-33% versus -32%), renin (-31% versus -27%) or aldosterone (-74% versus -61%) and pressor doses of NE (-55% versus -54%) or ANG II (-72% versus -44%) decreased by a comparable extent. Urinary PGE2 or PGF2 alpha were unchanged. These findings suggest that a high dietary sodium intake exerts a pressor effect in subjects with familial predisposition to essential hypertension. This pressor effect is not explained by an abnormal adaptation of body sodium, sympathetic activity, renin-angiotensin-aldosterone axis, cardiovascular pressor responsiveness and renal prostaglandin excretion to a high sodium diet.

Adult↗
PubMed1986

Familial Bartter's syndrome: report of a case with early manifestations and persistent hypercalciuria.

A case of familial Bartter's syndrome is reported. The child had early and severe clinical and biochemical manifestations. Indomethacin treatment effectively controlled the increased prostaglandin excretion but corrected only partially the potassium and the calcium losses. The child developed during treatment high serum calcium levels which were associated with high parathyroid hormone and calcitriol serum levels.

Bartter Syndrome↗
PubMed1985

Cytosolic free calcium and intracellular calcium stores in neutrophils from hypertensive subjects.

Alterations in intracellular calcium have been implicated in the pathogenesis of essential hypertension. To see whether this is a generalized phenomenon we assessed cytosolic free calcium and intracellular calcium stores in neutrophils from normo- and hypertensive subjects, by trapping the fluorescent calcium indicator quin2 in intact cells. Ten patients with untreated essential hypertension were compared with 10 age- and sex-matched normotensive subjects. The levels of cytosolic free calcium and intracellular calcium stores releasable by the calcium ionophore ionomycin did not differ. No significant relationship was found between blood pressure and the calcium parameters in all 20 subjects studied. The results indicate that essential hypertension is not associated with a membrane defect in calcium handling of all human cell systems, leading to generalized increases in resting values of cytosolic free calcium. Neutrophils do not appear to be a good model for intracellular calcium handling in vascular smooth muscle.

Adult↗
PubMed1985

Relationship of renal prostaglandins to distal transport of sodium chloride in normokalemic and hypokalemic man.

The relationship between renal prostaglandins (PG) and electrolyte transport in the thick ascending limb of Henle's loop (TALH) was examined in 8 normal subjects and in 7 patients with hypokalemia, the latter including 4 cases of Bartter's syndrome. Distal fractional delivery and distal reabsorption of chloride and sodium were determined using clearance techniques under maximal volume expansion, and urinary excretion rates of PGE2 and PGF2 alpha were measured. In the normal subjects, suppression of PG synthesis by indomethacin decreased distal delivery without changing distal reabsorption, suggesting that PG may influence solute transport at a site proximal to the diluting segment. In the subjects with Bartter's syndrome, however, distal reabsorption was impaired, this defect being apparently independent of PG as it was unaffected by inhibition of PG synthesis. In the patients with hypokalemia due to non-renal causes, distal reabsorption of chloride was increased, resulting in a decreased chloride clearance. These results suggest a link between renal PG and solute transport in normal man and also provide evidence that Bartter's syndrome is characterized by a prostaglandin-independent defect in distal reabsorption which is not found in hypokalemia due to other causes.

Absorption↗
PubMed1984

[Educating the hypertensive patient].

Patient education deserves to be placed on an equal footing with diagnosis and treatment in the prevention of hypertension. At the University Hospital of Geneva an education programme for hypertensive patients has existed for several years, with the object of improving long-term treatment compliance through better understanding and acceptance of the disease.

Humans↗
PubMed1984

Relationship of renal prostaglandins to three diuretics.

The effects of amiloride, a potassium-sparing diuretic, and of acetazolamide, a carbonic anhydrase inhibitor, were compared to those of triamterene, a potent prostaglandin stimulator which may result in acute renal failure after indomethacin pretreatment. Eighteen normal subjects on a constant sodium diet were given triamterene 200 mg/d, or amiloride 15 mg/d, or acetazolamide 750 mg/d for 3 days. Plasma potassium rose after triamterene and amiloride, and fell after acetazolamide. Natriuresis was increased after amiloride and acetazolamide, but not after triamterene. Plasma renin activity and urinary aldosterone were stimulated by the three diuretics. Triamterene induced a 4-fold increase in urinary prostaglandins E2 and F2 alpha and acetazolamide a 2-fold increase in prostaglandin E2 only, whereas amiloride showed no effect. No relationship was found between plasma or urinary electrolytes and urinary prostaglandins. Renal function was preserved in all cases. These results which show that amiloride, unlike triamterene, does not stimulate prostaglandins, suggest that nonsteroidal anti-inflammatory drugs (NSAID) which unmask triamterene nephrotoxicity may not constitute a hazard in association with amiloride. The prostaglandin response to acetazolamide may be indicative of adverse reactions during concomitant NSAID administration.

Acetazolamide↗
PubMed1984

Comparative therapeutic benefit of indomethacin, hydrochlorothiazide, and acetyl-salicylic acid in a patient with nephrogenic diabetes insipidus.

To define the importance of renal prostaglandins in nephrogenic diabetes insipidus (NDI), diuresis and the urinary excretion of PGE2 and PGF2 alpha were studied in a patient with NDI before and during inhibition of endogenous prostaglandin synthesis with either indomethacin (IND) or acetyl-salicylic acid (ASA). The excretion rates of PGE2 and PGF2 alpha were in the low normal range for the patient's age group, remained unchanged during 6 h of fluid deprivation and were suppressed by IND (150 mg/day), ASA (3 g/day), and by the combination of IND and hydrochlorothiazide (HCT, 50 mg/day). However, whereas IND, HCT, and the combination of IND and HCT reduced diuresis ASA did not. Free water clearance as determined during fluid deprivation remained positive during each phase of therapy. These data fail to demonstrate a direct effect of endogenous ADH on renal prostaglandin synthesis in NDI. The ineffectiveness of ASA to reduce diuresis indicates that indomethacin affects diuresis in NDI by a mechanism other than inhibition of cyclooxygenase.

Adolescent↗
PubMed1984

Cytosolic free calcium and intracellular calcium stores are normal in neutrophils from patients with essential hypertension.

Cytosolic free calcium and intracellular calcium stores were measured in neutrophils by trapping intracellularly the fluorescent calcium indicator Quin-2. Ten patients with untreated essential hypertension were compared to 10- age and sex-matched normotensive subjects. Intracellular calcium concentration and calcium stores did not differ in the two groups. No significant relationship was found between blood pressure and the calcium parameters. These results suggest that essential hypertension is not associated with a generalized cellular alteration in calcium handling.

Aminoquinolines↗
PubMed1983

[Endocrine function in old age (70 years and over)].

Internists are frequently faced with the problem of interpreting hormonal values and the results of endocrine tests in elderly patients. In this review, endocrine changes observed in the course of the ageing process are systematically examined for each endocrine gland. The causes of the modifications observed can for the sake of simplicity be classified into three types: 1. Reduction of the hormone's metabolism with, subsequent to its prolonged half-life, a reduction of secretion due to an appropriate feedback mechanism, without modification of the secretory capacity of the glands involved (e.g. thyroid hormones and cortisol). 2. Reduction of hormonal secretion as a consequence of loss of glandular mass (e.g. the gonads). 3. Changes in the sensitivity of target cells to a hormone (e.g. insulin, ADH, catecholamines, lactotrope cells, TRH and hypothalamus to steroids) due to either loss of receptors or modifications in post-receptor events.

Aged↗