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Biomedical subjects

M Andrejak

Publications and source records attributed to M Andrejak.

At least 73 records · Page 4Linked to original sources
PubMed1982

Cimetidine and circulating calciotropic hormone levels in uremic patients: evidence for a suppressive effect on calcitonin secretion.

The effect of oral cimetidine on parathyroid hormone and calcitonin plasma levels was evaluated in 12 uremic patients on chronic hemodialysis. Compliance to treatment was monitored by measuring cimetidine plasma concentrations. Plasma cimetidine was measurable in 7 patients and undetectable in 5. In compliant patients, there was no change in plasma concentration of calcium and parathyroid hormone but a significant fall of 75% in plasma calcitonin levels during treatment, followed by an increase towards initial values after cimetidine discontinuation. No significant change occurred in the other 5 patients. Cimetidine therefore appears to be of little value in the treatment of uremic hyperparathyroidism.

Adult↗
PubMed1981

[Control of hypertension and blood lactate during exercise. Comparison of central antihypertensive agents with the cardio-selective beta blockers metoprolol and atenolol].

To assess whether betablockers (BB) would better control blood pressure than central antihypertensive drugs (CAD) clonidine or alpha methyldopa in hypertensive patients during exercise, comparable triangular ergometric bicycle exercises were performed by the same patients while their hypertension had been controlled at rest either with CAD or BB. Blood pressure, heart rate and blood lactate before and during exercise were compared in II patients treated with metoprolol and CAD, and in 12 other patients treated with atenolol and CAD. Systolic and diastolic blood pressure on exercise were significantly lower with BB than with CAD. Heart rate and rate-pressure product were always lower with BB than with CAD. Blood lactate increase was greater with BB than with CAD. The work capacity was greater with atenolol than with CAD, but comparable between metoprolol and CAD.

Adrenergic beta-Antagonists↗
PubMed1981

[Diuretics and vascular risk factors. Comparison between tienilic acid and chlorothiazide (author's transl)].

Tienilic acid (250 mg/day) was compared with chlorothiazide (500 mg/day) in 25 hypertensive patients in a randomized cross-over study (2 periods of 2 months). Mean supine arterial pressure was lower with tienilic acid than with chlorothiazide (106 +/- 3 vs 111 +/- 3 mm Hg, p less than 0.05) whereas no difference could be noted in body weight, natriuresis and plasma renin activity. Glucose tolerance tests were altered in the same fashion. Serum cholesterol (234 with tienilic acid and 239 mg/dl with chlorothiazide) and serum triglyceride levels (178 with tienilic acid and 179 mg/dl with chlorothiazide) were not different. Serum urate concentrations were lower with tienilic acid (4.8 mg/dl) than with chlorothiazide (7.8 mg/dl) whereas fractional excretion of urate was much higher with tienilic acid (17 +/- 2%) than with chlorothiazide (7 +/- 2%). Thus, the only metabolic advantage of tienilic acid over chlorothiazide is its hypouricemic effect which warrants long term studies to evaluate its vascular prognostic significance.

Adult↗
PubMed1981

Blockers of beta and H2 receptors and secondary hyperparathyroidism in uraemia.

The suppressive effect on PTH secretion of propranolol, a beta 1 and beta 2 blocker, and that of atenolol a specific beta 1 betablocker was compared in 24 uraemic patients not yet on dialysis in a cross over study. Although plasma PTH concentrations were comparable, plasma bicarbonate was higher with propranolol suggesting that the initial suppression of PTH secretion by propranolol was greater as a higher bicarbonate should lead to lower ionised calcium. The suppressive effect of cimetidine on PTH secretion was assessed in 12 patients on chronic haemodialysis. In the seven compliant patients there was no change in N and C terminal plasma PTH values but plasma calcitonin concentrations significantly decreased with cimetidine and returned to initial values after cimetidine was discontinued.

Adult↗
PubMed1980

[Pharmacologic study of several alpha-adrenolytics].

Six alpha-adrenoceptor blocking agents have been investigated in dogs and rats. 170 150 and 170 153 have been found the most potent of these agents. At low doses (0,1 microgram/kg) they reversed the pressor response to low doses of adrenaline (0,1 and 0,3 microgram/kg) and suppressed the response to high doses of adrenaline. They reduced the pressor response to noradrenaline. In addition, in dogs 170 150 increased the tachycardia caused by stimulation of the cardiac nerve. The compound prevented and reversed the inhibition caused by clonidine on the effects of cardiac nerve stimulation. 170 153 did not increase the tachycardia caused by cardiac nerve stimulation, but it prevented and reversed the inhibitory effects of clonidine on this stimulation. The results show that 170 150 and 170 153 are potent alpha-adrenoceptor blocking agents acting on both pre and post-synaptic alpha-adrenoceptors which could be interesting pharmacological tools.

Adrenergic alpha-Antagonists↗
PubMed1980

Effect of propranolol and metoprolol on parathyroid hormone and calcitonin secretions in uraemic patients.

Nine uraemic patients not being treated by dialysis received intravenous propranolol 1 microgram/kg/min for 85 minutes after a priming dose of 1 mg. Fifteen days later, six of them received intravenous metoprolol 1.2 microgram/kg/min after a priming dose of 1.2 mg. Plasma concentrations of parathyroid hormone (PTH) and calcitonin fell significantly after propranolol but not after metoprolol, whereas no change in plasma concentrations of ionised calcium and phosphate occurred with either drug. Heart rate fell similarly with both drugs. The fact that propranolol acutely suppressed PTH and calcitonin secretion in uraemic patients indicates that further studies are warranted to assess the long-term effects of the drug on the secretion of these hormones and on renal osteodystrophy. The contrast between the responses to propranolol and metoprolol supports the concept that PTH and calcitonin secretion is modulated through specific beta 2-receptors.

Adult↗
PubMed1980

Value of combined intravenous renal arteriography and pyelography in the diagnosis of renovascular hypertension.

1. The technique of combined intravenous renal arteriography and pyelography is described and results in 848 hypertensive patients are reported. 2. The procedure was tolerated better than Seldinger arteriography and the diagnostic accuracy for renal artery stenosis was 95%. 3. The prevalence of renovascular disease was 7%. 4. Cost-effectiveness calculations favour combined intravenous arteriography and pyelography rather than the usual approach based on assessment of the indications for Seldinger arteriography from clinical and urographic signs.

Cost-Benefit Analysis↗
PubMed1980

[Evidence, in uremic man, of the role of beta 2 adrenergic receptors in the secretion of parathyroid hormone and calcitonin (author's transl)].

In order to determine the effect of beta-blocking agents on secretions of parathyroid hormone and calcitonin, 9 patients with renal failure were given single doses of propranolol (a blocker of the beta 1 and beta 2 receptors) or an equivalent amount of metoprolol (a beta 1 selective agent). Propranolol causes a decrease of plasma parathyroid hormone (p less than 0.02) as well as of calcitonin (p less than 0.05) whereas metoprolol has no effect on the plasma levels of these hormones. These findings suggest that parathyroid tissue and thyroid C cells have receptors that are exclusively of the beta 2 type which are modulating the secretion of parathyroid hormone and calcitonin.

Adult↗
PubMed1977

[The sympathetic nervous system inhibition in the antihypertensive effect of beta-blockers (author's transl)].

The decrease of sympathetic activity by the beta-blocking drug, as demonstrated by the decreased electric activity of the splanchnic nerve and by the decreased urinary catecholamine reponse to tilt as well as by the decreased levels of plasma dopamine beta-hydroxylase exists not only in hypertension with elevated PRA but also in hypertension with normal or low PRA. In these latter cases the antihypertensive effect is better explained by the decrease in the sympathetic nervous system activity than by the decrease of PRA. This effect seems to be indirect and probably, as suggested by Lewis, as a result of damping sensory input to the central nervous system from the heart, whose capacity to respond to exercice and stress is blunted by beta-adreno-receptor blockade.

Adrenergic beta-Antagonists↗
PubMed1977

[Systemic arterial hypertension: pathogentic role of the sympathetic nervous system].

Role of the clinical and experimental data suggesting the role of the sympathetic nervous system in some essential hypertension are reviewed: increase in heart rate and diastolic blood pressure during orthostatism, increase in cardiac output resulting from increase in cardiopulmonary blood volume and/or in myocardial contractility, increase in peripheral resistances, elevated plasma catecholamines and dopamine-bêta-hydroxylase, disturbances in arterial baroreceptor sensitivity and in vascular response to adrenergic stimuli, elevated plasma renin activity. It appears that the role of a sympathetic overactivity is mainly important in labile hypertension with hyperkinetic syndrome and elevated plasma renin activity.

Animals↗
PubMed1974

[Cryoglobulinemia].

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Blood Protein Disorders↗