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Biomedical subjects

J Sassard

Publications and source records attributed to J Sassard.

At least 217 records · Page 12Linked to original sources
PubMed1977

Pharmacokinetics of atenolol in patients with renal impairment.

The pharmacokinetics of atenolol, a new cardioselective beta-adrenoceptor blocking agent, were determined following both acute and chronic dosing in 33 hypertensive patients with widely differing levels of renal impairment. In patients with normal renal function the atenolol half-life was calculated to be about six hours following single 100 mg oral doses. This value increased markedly in patients with renal insufficiency and the blood clearance of atenolol was found to have a significant correlation with the glomerular filtration rate. This demonstrated the importance of the kidneys in the elimination of the drug. After 8 weeks oral treatment with atenolol (100 mg twice daily) a significant decrease in blood pressure, heart rate and plasma renin activity was observed, but no correlation was established between the blood levels of atenolol and any of its pharmacodynamic effects. A positive correlation was found however between the anti-hypertensive action of atenolol and the pretreatment value of the plasma renin activity.

Atenolol↗
PubMed1976

Plasma renin activity as a function of age in two new strains of spontaneously hypertensive and normotensive rats.

1. Strains of spontaneously hypertensive and normotensive rats were selected by repeated inbreeding. 2. Brief ether anesthesia was shown to produce a two- to three-fold increase in plasma renin activity in both strains. 3. Plasma renin activity was significantly higher in young spontaneously hypertensive than in normotensive rats of the same age (5-7 weeks). After the ninth week plasma renin activity decreased and, at week 45, became significantly lower in hypertensive than in normotensive rats. 4. When hypertension was established a significant inverse relationship was found between plasma renin activity and systolic blood pressure in spontaneously hypertensive and in normotensive rats. 5. It seems unlikely that the renin-angiotensin system plays a major role in the maintenance of the established spontaneous hypertension in this strain. However, renin hypersecretion may be important in the early pre-hypertensive stage of genetic hypertension in rats.

Aging↗
PubMed1976

Effect of sodium restriction and angiotensin II infusion in Bartter's syndrome.

Five patients with Bartter's syndrome were investigated. Sodium restriction (less than 10 mEq/day for at least 5 days) showed a renal sodium wastage in only two patients (I and II) in spite of increased aldosterone secretion rate (from 151-427 to 680-842 mug/day). The effect of angiotensin II (A II) 80ng/kg/min for 30-180 min, on plasma renin activity (PRA), plasma aldosterone, and urinary sodium excretion was compared with the effect of a previous infusion of 5% dextrose given at the same rate, 0.5 ml/min for 1 hr. A II infusion resulted in increased plasma aldosterone levels: from 236-330 pg/ml to 800-881 pg/ml in 30 min. This increase was also observed in patient II (from 139 to 600 pg/ml). PRA was decreased by A II infusion (from 1,142-2,462 to 121-1,625 ng/liter/min). In patient IV, this decrease in PRA was also observed when he was on a salt-restricted diet (from 1,934 to 370 ng/liter/min); but the minimal PRA was still higher (370 ng/liter/min) than with a normal diet (121 ng/liter/min). In no case could normal PRA level be obtained. A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80-90 to 265-230 muEq/min in 30 min). Urinary sodium excretion decreased in the other patients from (37.5-213 to 4.30-46 muEq/min) and fractional sodium excretion was reduced in patient V (from 0.56% to 0.45% at 30 min and to 0.29% at 120 min). No significant change with A II infusion was observed in patient IV when he was on a sodium-restricted diet (from 1 to 2.5 muEq/min in 30 min). Urinary potassium excretion was similar to sodium excretion. No change was observed in plasma potassium and sodium.

Aldosterone↗
PubMed1976

A kinetic study of plasma renin and aldosterone during changes of posture in man.

Cardiovascular parameters, hematocrit (Ht), plasma electrolytes, renin activity (PRA) and aldosterone concentration (PAC) were measured in 12 normal human subjects (6 males and 6 females) eating an ad lib diet. At 8 AM, volunteers assumed the following postural changes: 1 hour supine, then 2 hours upright and finally 1 hour supine. Orthostatism induced the following changes: heart rate, systolic and diastolic blood pressure increased immediately; Ht rose significantly at the 5th min in males but not in females; Plasma sodium showed no variations but potassium increased after 30 min; PRA rose significantly at the 5th min and, after 120 min of orthostatism, was found to be 3 times greater than its value after recumbency; and PAC increased significantly at the 15th min and exhibited a plateau 4.5 times its basal values after 90 min of upright posture. When subjects returned to the supine position all the parameters, except PAC decreased. During active orthostatism, a significant correlation was found between PAC and plasma potassium, but correlation was closer between PAC and PRA and between PAC and PRA + potassium. It can be concluded that the renin-angiotensin system is a more potent stimulus for aldosterone secretion than plasma potassium in normal man assuming postural changes. The results presented here can be applied to the development of a short posture test in non-hospitalized patients.

Adult↗
PubMed1976

Effects of right atrial stretch on plasma renin activity.

In anaesthetized dog, right atrial stretch leads in the first five minutes to a decrease in plasma renin activity, when measured in inferior vena cava just above the renal veins. Bilateral cervical vagotomy increases plasma renin activity. After vagotomy, atrial stretch no longer has any effect on plasma renin activity. The results support the hypothesis of a control of renin secretion originating from atrial volume receptors.

Animals↗
PubMed1976

Acute renal effects of new beta-adrenergic receptor site blocking agents on renal function.

The effects of two new beta blockers on renal function have been studied. There were significant decreases in urine flow, urea clearance, sodium and chloride excretion rates after acute administration. Fractional excretion of sodium (FeNa) fell significantly but did not continue to fall during chronic administration. Blood pressure and plasma renin activity decreased significantly after two months' therapy. These findings suggest that beta blockers in patients with unstable cardiovascular function increase the need for concomitant diuretic therapy.

Acebutolol↗
PubMed1975

[Bartter's disease associated with hypercorticism, phosphate and magnesium deficiencies and familial renal tubular disease].

A new case of Bartter's syndrome is described. There is a context of other cases of familial renal tubular disease with a sex-linked heredity. In this case, the Bartter's syndrome is associated with magnesium deficiency and hypomagnesemia, with a ricket and severe phosphate deficiency, and finally with an hypercorticism. The basal secretion rate of cortisol agree with a Cushing's syndrome. This hypercorticism is corrected by aminogluthetimide. The influence of the hyperreninism on the hypercorticism is discussed.

Adrenocortical Hyperfunction↗
PubMed1974

Vascular reactivity in spontaneously hypertensive normotensive and hypotensive rats.

1 Three strains of rats spontaneously hypertensive (HRS), normotensive (NS) and hypotensive (HOS), were selected by repeated inbreeding.2 In order to explain the different blood pressure levels observed, we have studied their vascular reactivity to noradrenaline and angiotensin II. Experiments were performed in anaesthetized ganglion-blocked, vagotomized rats.3 The reactivity to noradrenaline was significantly higher in HRS than in NS and HOS rats.4 The reactivity to angiotensin II appeared identical in the three strains used.

Angiotensin II↗