Biomedical subjects
A Helber
Publications and source records attributed to A Helber.
[The addicted alcoholic in the hospital].
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[The anxieties of sick persons].
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[Support for the dying--assistance in dying, where is the limit?].
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Cardiovascular and adrenal sensitivity to angiotensin II in essential hypertension.
Regulation of aldosterone secretion by sodium chloride is impaired in a group of essential hypertensives: high-salt diet fails to suppress aldosterone in these patients despite low renin values. The mechanism of this impaired regulation of aldosterone has not been clarified so far. We tested the sensitivity of aldosterone secretion and blood pressure to A II in 20 normotensive controls (aged 20-60, MAP 92 +/- 3 mm Hg), in ten normotensives with one or two parents with hypertension, and in 21 patients with essential hypertension (aged 17-65, MAP 119 +/- 4 mm Hg). After a period of 6 days on high-salt intake (300-320 mEq Na+/day), A II (0.1, 0.5, 1.0 and 2.0 ng/kg/min) was infused, each concentration for 30 min. According to aldosterone excretion during sodium loading, patients were divided into group A with complete suppression (n = 12, aldosterone excretion 3.6 +/- 0.4 microgram/day) and in group B with insufficient suppression (n = 9, aldosterone excretion 15.5 +/- 2.3 micrograms/day). Despite similarly low plasma renins, rise of serum aldosterone levels during A II infusion was significantly higher in group B patients than in group A patients and normotensive controls. Rise in mean arterial blood pressure, however, brought about by graded A II infusion was similar in both groups of hypertensives and in normotensive controls. The results demonstrate an increased adrenal sensitivity to A II in a subgroup of essential hypertensives only. A similar adrenal hypersensitivity to A II found by others in patients with hyperaldosteronism due to adrenal hyperplasia supports the hypothesis that the same mechanism underlies both disorders.
[Primary hyperaldosteronism: differentiation between aldosterone-producing adenoma and idiopathic adrenocortical hyperplasia (author's transl)].
The regulation of aldosterone secretion by sodium restricted and enriched diet was assessed in 21 patients with primary aldosteronism for differentiation between unilateral aldosterone-producing adenoma and adrenocortical hyperplasia causing autonomous aldosterone hypersecretion. Compared to 10 patients with idiopathic adrenocortical hyperplasia, urinary aldosterone excretion after 4 days of sodium restricted diet was significantly higher in 11 patients with established adenoma (41.3 +/- 16.3 micrograms/24 h vs 19.8 +/- 8.5 micrograms/24 h; P less than 0.005). After six days of sodium loading these differences became even more obvious (35.3 +/- 14.0 micrograms/24 h vs 12.7 +/- 3.7 micrograms/24 h; P less than 0.0005). Sodium excretion did not influence aldosterone secretion in the adenoma group. In patients with hyperplasia both parameters showed a negative correlation (r = -0.522; P less than 0.001). Differentiation without overlap between both patient groups was achieved by comparison of the quotient of aldosterone excretion and serum potassium level during sodium enriched diet.
Antihypertensive effects of captopril and saralasin in essential and renal hypertension.
The antihypertensive effect of captopril and its mechanism of action were studied in patients with essential and renal hypertension. In mild essential hypertension (n = 12), during monotherapy with captopril (50 to 450 mg, 4 to 12 weeks) blood pressure was normalized in seven, improved in two and remained unchanged in three patients, plasma levels of active and acid-activatable inactive renin significantly increased and angiotensin II decreased, whereas no consistent changes in urinary kallikrein excretion occurred. In severe renal (n = 14) and essential (n = 9) hypertension, blood pressure was normalized in eight (seven with renal hypertension), improved in seven and unchanged in eight patients, when captopril (50 to 450 mg, 3 to 15 months) was added to the antihypertensive medication. In one patient with stenosis in a transplanted renal artery reversible renal failure occurred during captopril therapy possibly because of a steep initial decrease in blood pressure, although a toxic effect of the drug cannot be excluded. In another series of 12 renal and 8 essential hypertensive patients, a significant correlation between the acute effect of captopril (within 90 minutes) an saralasin on blood pressure was demonstrated (r=0.71, p less than 0.001). The change in blood pressure after either drug was significantly related to the initial plasma renin concentration. In conclusion, captopril seems to be an effective antihypertensive agent in essential and renal hypertension. Renal function should be monitored during captopril therapy. Our studies suggest that captopril decreases blood pressure by inhibiting the vasopressor action of the renin-angiotensin system.
Characterization of a group of essential hypertensives with impaired regulation of aldosterone.
The pattern of aldosterone excretion during high sodium intake in 100 patients with essential hypertension allowed the differentiation of two groups: in the majority of patients (group A, n = 64) aldosterone excretion was suppressed below 6 micrograms/day similar to the normotensive control group. In a second group (group B, n = 36), aldosterone remained above the control range despite forced sodium loading. In group B, serum potassium was significantly lower than in patients of group A (3.81 +/- 0.44 meq/l vs. 4.26 +/- 0.57 meq/l, p less than 0.001). The blood pressure lowering effect of spironolactone (200 mg/d) was more pronounced among patients in group B. Plasma renin values tended to be lower in group B compared to patients with suppressed aldosterone. Infusion of Angiotensin II (0.1 - 2 micrograms/kg/min) led to a similar relative rise of plasma aldosterone levels in both groups despite higher baseline values in group B. The exact mechanism of the impaired regulation of aldosterone in a subgroup of patients with essential hypertension remains to be elucidated.
[Clinical aspects and treatment of the hypertensive emergency (author's transl)].
The term "hypertensive emergency" includes all clinical syndromes which are triggered by a rapid rise in the arterial blood pressure and are improved by medicinal lowering of the blood pressure. Among them are hypertensive encephalopathy, acute rise in blood pressure with left heart failure and acute rise in blood pressure complicated by intracerebral hemorrhage or a dissecting aortic aneurysm. Parenteral application of dihydralazine, diazoxide and clonidine are suitable for immediate lowering of blood pressure medicinally and sodium nitroprusside under clinical supervision. In phaeochromocytoma Regitin is the drug of choice.
[Increased cardiovascular arteriosclerosis risk in patients with analgesic nephropathy (author's transl)].
The retrospective investigation of 54 patients with analgesic nephropathy showed the relatively early occurrence of coronary sclerosis and an increased frequency of arteriosclerotic renal artery stenosis. Angina pectoris was found in 14 patients with a mean age of 48 1/2 years. Summation of risk factors is the probable cause of the tendency for arteriosclerosis: hypercholesterolaemia and hypertriglyceridaemia was found in 29 patients, arterial hypertension in 42 patients, which was so severe in half of the patients that combined treatment with two or more drugs was necessary. The causes of lipid metabolism disturbances as well as the pathogenesis of arterial hypertension are not known. Arteriosclerotic renal artery stenoses observed in 8 patients are not likely to be the cause of hypertension.
Na-K-ATPase in erythrocyte ghosts is not a marker for primary hypertension.
In search for a diagnostic marker for essential hypertension, we investigated the activity of the ouabain sensitive Na-K-ATPase and the ouabain insensitive ATPase in erythrocyte ghosts of 57 patients with essential hypertension, 12 patients with renal hypertension, 6 patients with Cushing's syndrome and 4 patients with primary hyperaldosteronism. Na-K-ATPase-activity was increased in patients with essential hypertension and in patients with renal hypertension compared with controls with a considerable overlap. Na-K-ATPase-activity was increased in all patients with Cushing's syndrome but was not different from the control group in patients with Conn's syndrome. Ouabain-insensitive ATPase-activity was similar in all patients and in normotensive controls. The serum of patients with essential hypertension did not exhibit an ouabain-like ATPase-inhibiting activity when incubated with erythrocyte ghosts of normotensive controls. In our hands, determination of the Na-K-ATPase-activity in erythrocyte ghosts cannot be used as a diagnostic marker for essential hypertension.
[Effect of saralasin on blood pressure, plasma renin and plasma noradrenaline in hypertensive patients].
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[Hypotensive effect of spironolactone in patients with essential hypertension and aldosterone regulation disorders].
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Evidence for a subgroup of essential hypertensives with non-suppressible excretion of aldosterone during sodium loading.
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Increased activity of the Na-K-ATPase in red cell-ghosts of patients with Cushing's syndrome: possible significance for the pathogenesis of glucocorticoid-induced hypertension.
The Na-K-ATPase activity of erythrocyte ghosts was increased in 6 patients with Cushing's syndrome compared with 28 control subjects (0.986 +/- 0.291 versus 0.259 +/- 0.1 microM Pi . h-1 . mg-1, p less than 0.001). Ouabain insensitive Mg-ATPase activity was similar in both groups. These data support the concept of an activation of the Na-pump in patients with glucocorticoid excess.
[Spironolactone in essential hypertension associated with abnormal aldosterone regulation and in Conn's syndrome (author's transl)].
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Effects of a beta 1-selective adrenergic agonist in normal human volunteers.
In healthy volunteers, the effects of prenalterol, a new beta 1-adrenoceptor agonist, on renal hemodynamics, excretory function, plasma-renin-activity, plasma cAMP concentration, and plasma and urinary norepinephrine were studied. Besides an increase in blood pressure, which was adjusted to about 20 mmHg above the resting values, and an increase of heart rate, prenalterol induced only transient decreases of urinary volume and free water clearance and in increase of sodium excretion. The other parameters measured did not change. Thus prenalterol mainly exerts positive inotropic and chronotropic effects and does not affect renal circulation.