[Self-measurement of blood pressure].
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Biomedical subjects
Publications and source records attributed to M Anlauf.
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To determine the beta-adrenoceptor subtype controlling renin release from the kidneys, several beta-adrenoceptor subtype selective agonists and antagonists were administered to 15 healthy volunteers. While isoprenaline infusion (1, 2 and 4 micrograms/min for 5 min each) markedly increased plasma renin activity (PRA), the beta 2-selective agonist fenoterol failed to change PRA. The isoprenaline induced rise in PRA could be completely prevented by the beta 1-selective antagonists metoprolol (10 mg i.v. 45 min prior to isoprenaline infusion) and betaxolol (5 mg i.v. 45 min prior to infusion) indicating that renin release is mediated by beta 1-adrenoceptors. Binding studies with the highly specific beta-adrenoceptor radioligand (+/-)-125iodocyanopindolol demonstrated that membranes from human kidney cortical slices contain predominantly, if not exclusively, beta 1-adrenoceptors. These in vivo and in vitro results support the view that the beta-adrenoceptor mediating renin release from the human kidney is of the beta 1-subtype.
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In 36 healthy subjects of various ages (14-76 years) the number of alpha 2-adrenergic receptors in platelets - as determined by [3H]yohimbine binding - and plasma catecholamine levels were measured. A highly significant negative correlation (r = -0.666, P less than 0.001) between the number of alpha 2-adrenergic receptors and age was found; on the contrary, plasma catecholamine concentrations increased with increasing age. Thus, reduced responses in the elderly to adrenergic stimuli may be due to reduced number of adrenergic receptors.
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Errors in the treatment of hypertension may occur at any level of the therapeutic concept. They can, however, largely be avoided by considering the following suggestions. A hypertension requiring treatment is usually only detectable by several blood pressure measurements taken on different days. A diagnostic confirmation of the hypertensive disease should precede the onset of the antihypertensive therapy. General measures and dietetic restrictions and indispensable to any hypertensive therapy. Drug therapy can only be successful if it is individual, if side-effects are avoided and if contraindications are taken into consideration. In addition the frequency of taking the drug and the necessary number of tablets to regulate the blood pressure must be kept as low as possible.
A diagnostic examination may be called rational if it leads to a short, less costly and especially more certain diagnosis for the patient. Among other things, sensitivity and specificity, i.e. the proportion of correct positive to correct negative results of the separates steps of the examination determine the reliability of the answers to diagnostic questions. In most hypertensive patients the diagnosis can be completed in medical general practise. First results in West Germany show that only about 5 to 10% of patients require further investigations in special practices, general hospitals or special departments.
In 13 hypertensive patients taking the beta-receptor blocker atenolol, EEG and behaviour effects were studied. Using a single-blind sequential trial design, a 5-d placebo period was followed by a 6-d atenolol treatment period (100 mg/d). During either treatment period, two examinations yielded data derived from neurophysiological, test-psychological, and cardiovascular measurements. The statistically significant changes due to atenolol therapy indicated an improvement of vigilance, a smooth anxiolytic and tranquilizing effect, and at least no negative influences on discriminatory reaction time and concentration ability. The primary therapeutic effects were significant falls in systolic and diastolic blood pressure as well as in pulse rates. The study is still in progress and will be completed after 20 patients are reached. The data will then be reanalyzed in order to get further insight into CNS effects of a beta-blocking therapy concerning favorable vs. poor drug responders.
19 conventional and 19 electronic blood pressure measuring devices were tested on a average of 23 patients each. The patients were classified according to age, sex, and experience in blood pressure measurement. Altogether, the accuracy of the electronic devices was inferior to that of the conventional apparatus. Especially the diastolic blood pressures were estimated considerably too low by the electronic devices. Furthermore, these instruments were more sensitive to a false position of the microphone membrane than the conventional devices and they showed, in the average, greater differences between two exemplars of the same instrument. Blood pressure readings with conventional devices were significantly influenced by the patients' experience (systolic blood pressure) and age (diastolic blood pressure), whereas the readings with electronic machines were significantly affected by the patients' sex (systolic and diastolic blood pressure) and age (diastolic blood pressure). The result of the technical development of blood pressure devices for self-measurement is rather disappointing, especially with respect to costs and benefits.
Chronic beta-blockade with the cardioselective blockers practolol and atenolol had no attenuating effect on blood-pressure increases provoked by cold pressor test or by plasma expansion. Reports in the literature of an exaggerated cold pressor test reaction under propanolol therapy could be confirmed with practolol and atenolol. This may be regarded as an advantage of cardioselective blockade. The increase of the cardiac output after plasma expansion is enhanced during cardioselective beta-blockade. This could result from a reduced action of cardioselective blockers on the capacitance vessels. Concerning the mechanisms of antihypertensive action of beta blocking agents our findings do not support the cardiac output hypothesis. Before and during beta blocking therapy baroreflex sensitivy was not significantly different. So the baroreflex theory can't be strengthened neither.
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Between 1972 and 1976 15 patients with chronic renal failure of different aetiology and varying severity were observed who developed 23 hypercalcaemic phases during treatment with calcium-containing drugs. 12 instances of hypercalcaemia occurred during conservative treated during conservative treatment (serum creatinine 177-1061 mumol/l, equivalent to 20-120 mg/l) and 11 during chronic haemodialysis (serum creatinine 707-1061 mumol/l, equivalent to 80-120 mg/l). In 15 cases hypercalcaemia was caused by a hexacalciumhexasodium-heptacitratehydrate complex (Acetolyt), in 6 cases by the combined use of this drug with calcium ion-exchange resins on a calciumpolystyrolsulfonate base, and in two cases by the use of calcium tablets and calciumpolystyrolsulfonate, respectively. The daily doses of these drugs were in the usual therapeutic range in most cases. Deterioration of renal function was observed in two cases and coma in a further two cases. In 5 cases gastric ulcers were demonstrated. Three patients died. In no patient was there evidence of florid hyperparathyroidism. Treatment with calcium-containing drugs in patients with renal failure should only be carried out under regular control of calcium concentrations.
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Out of 14 women with acute intermittent porphyria seven were treated for an average of five years with ovulation inhibitors. In another two cases a bilateral surgical oophorectomy and a radiotherapeutic castration were performed. Five untreated women formed the control group. In contrast to the control group there were no further acute exacerbations in the group treated with oral contraceptives. The two patients with oophorectomy and irradiation castration died following multiple acute exacerbations. In four of the women treated with oral contraceptives the development of persistent, and in some cases severe, arterial hypertension was observed. The pathogenesis cannot be explained.
In 17 patients (15 women, 2 men) with acute intermittent porphyria in the incidence of 23 clinical symptoms during 49 attacks was calculated. The most frequent symptoms in percentage of attacks were: Red colour of the urine 100%, abdominal pain 92%, tachycardia 88%, hypertension 75%, vomiting 54%, peripheral neuropathy 50%. In 35% of acute attacks a transient normochromic, normocytic anemia developed which is probably due to a disturbance of heme synthesis. Oliguria was found in 25%, azotemia in 12.5% of attacks. 4 patients with an average of 5 preceding acute attacks showed a persistent reduction of renal function during the symptom-free interval, in contrast to 12 patients with an average of 1.7 previous attacks and normal renal function. During the observation period from 1960-1974 3 (= 18%) of the 17 patients died.
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