PubMed Health⌕ Search

Biomedical subjects

E Fritschka

Publications and source records attributed to E Fritschka.

At least 37 records · Page 2Linked to original sources
PubMed1992

Comparisons of once-daily nilvadipine with enalapril and diuretic in patients with essential hypertension.

The antihypertensive efficacy of the new dihydropyridine derivative nilvadipine given once daily was compared in two randomized, double-blind studies with that of hydrochlorothiazide/triamterene (HCT/T) and of enalapril. In the first study, arterial pressures were compared after 4 weeks of therapy with nilvadipine (16 mg q.d.) or HCT/T (25/50 mg q.d.) in patients with mild-to-moderate hypertension in a parallel-group design. The combination of both treatments was administered after 4 weeks if diastolic arterial pressures were > 90 mm Hg. The blood pressure (BP) in the nilvadipine group (n = 125) was 161/102 +/- 17/7 (mean +/- SD) mm Hg after a 2-week placebo period and decreased after 4 weeks by -16/-13 +/- 22/12 mm Hg. The BP decreased in the HCT/T group (n = 124) compared to the nilvadipine group to a similar degree (p = 0.91, n.s.) from 160/103 +/- 17/8 mm Hg by -17/-13 +/- 18/11 mm Hg. A combination therapy was started after 4 weeks in 39 patients in the nilvadipine group and in 34 patients in the HCT/T group. This led independently of the treatment sequence, to a similar decrease in BP in the nilvadipine group (-17/7 +/- 16/10 mm Hg) and in the HCT/T group (-12/9 +/- 16/9 mm Hg). In the second study, the antihypertensive effect of nilvadipine (1 x .8 mg) was compared with that of enalapril (1 x 10 mg) in a randomized, double-blind, crossover design. Sixty-one patients with essential hypertension (WHO I-II) were treated over two 4-week periods following placebo periods of 2 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗
PubMed1992

Lack of oral kallikrein in lowering systemic blood pressure in primary hypertension.

Primary hypertension is associated with a lack in renal kallikrein activity which might be one of the reasons for the blood pressure elevation. Some smaller and partially uncontrolled studies suggested that an oral substitution of glandular kallikrein lowers blood pressure by a kinin-mediated vasodilation and increased natriuresis. To test this hypothesis we treated in two studies over 100 patients with untreated mild to moderate primary hypertension (WHO I-II) for 5 resp. 12 weeks in a double blind randomized and placebo controlled manner with 1800 U glandular kallikrein orally. Blood pressure measurements were performed according to the two study designs after 3 and 5 resp. 8 and 12 weeks of treatment sphymomanometrically in the day time course. No significant changes in blood pressure by kallikrein treatment could be observed at any time. Neither renal kallikrein excretion, renin and ACE-activity nor blood glucose concentration in diabetics or non-diabetics was changed. Thus, we could undoubtedly demonstrate that oral applied glandular kallikrein has no effect on primary hypertension.

Administration, Oral↗
PubMed1991

[Effect of erythropoietin therapy on alpha receptor density in chronic dialysis patients].

The effect of a six months therapy with human recombinant erythropoietin (rHu-EPO) on blood pressure and on several parameters of sympathetic nervous activity was studied in chronic haemodialysis patients in a controlled and randomized trial in order to gain further insight into the mechanism of rHu-EPO-induced blood pressure elevation. Treatment was started at a dose of 3 X 80 IE/kg/week in eleven patients aiming to increase the initial hemoglobin concentration (7.0 +/- 0.3 [SEM] g%) to 10.0 g% by dose adjustments, while another untreated eleven patients served as a control group. Diastolic arterial pressure measured before and after haemodialysis increased on rHu-EPO treatment by 7 and 8 mm Hg respectively (p less than 0.05). Plasma noradrenaline concentration was increased (p less than 0.05) after the six months treatment period in the presence of unchanged dry weights. Conversely platelet alpha 2-adrenoceptor density (3H-yohimbine binding) and the fraction of high affinity binding sites for alpha 2-agonists (3H-UK 14.304) decreased (p less than 0.01) along with a decrease in reactivity to exogenous noradrenaline (p less than 0.05). None of these parameters changed in the control group compared to pretreatment values. The results obtained demonstrate that increased plasma noradrenaline concentrations may participate in rHu-EPO induced blood pressure increases. The decrease in platelet alpha 2-adrenoceptor densities and the decrease in noradrenaline reactivity in the presence of increased plasma noradrenaline concentrations suggest an intact regulation of alpha 2-adrenoceptors in chronic haemodialysis patients on chronic rHu-EPO therapy.

Blood Platelets↗
PubMed1990

Effect of erythropoietin on parameters of sympathetic nervous activity in patients undergoing chronic haemodialysis.

The effect of erythropoietin (rHu-EPO) on blood pressure and on parameters of sympathetic nervous activity of patients undergoing chronic haemodialysis treatment was evaluated in a controlled and randomized 6-months study. Both groups did not differ significantly at the onset of the study in terms of dialysis protocol, haematological parameters, blood chemistry, weight, blood pressure and parameters of sympathetic nervous activity. Haemoglobin increased from 7.0 +/- 0.3 g dl-1 to 10.0 +/- 0.3 g dl-1 by 6 months on rHu-EPO (n = 11) and remained constant in the control group (n = 11). After 6 months diastolic blood pressure was higher in the treatment group compared with the control group as well as compared with pretreatment values, whereas reactivity to exogenous noradrenaline and platelet alpha 2-adrenoceptor densities ([3H]-yohimbine- and [3H]-UK 14,304-binding sites) were lower. Plasma noradrenaline concentration increased during rHu-EPO compared with pretreatment values, while dry weights were unchanged during the study. The results demonstrate alterations of some parameters of sympathetic nervous activity during rHu-EPO-therapy which were absent in the control group.

Blood Platelets↗
PubMed1990

Twenty-four-hour profiles of growth hormone, prolactin and cortisol in the chronic vegetative state.

The 24-h profiles of growth hormone (GH), prolactin (PRL) and cortisol were obtained from 11 patients in the chronic vegetative state in order to gain more insight into the neuroendocrine alterations caused by widespread suprahypothalamic brain damage. Age and sex-matched normal subjects served as a control group. Patients had fewer high-amplitude GH peaks (greater than 20 mU/l: 6 peaks/24 h vs 21 peaks/24-h in controls) and a (non-significant) tendency towards higher basal GH concentrations. PRL concentrations were higher in patients (296 +/- 212 (SD) vs 120 +/- 28 mU/l). Cosinor analysis also showed that 24-h rhythmicity was preserved, but acrophases were more dispersed. A nocturnal PRL acrophase occurred in only three of 11 patients but in 10 of 11 control subjects. The number of PRL peaks was the same in patients and controls. Cortisol concentrations were also higher in patients (298.3 +/- 114.6 vs 193.6 +/- 97.4 nmol/l) with a preserved circadian rhythm. The acrophases, however, were likewise more dispersed. There was no difference in the number of cortisol peaks between patients and controls, but the mean peak duration was shorter in patients (75.4 +/- 28.1 vs 109.5 +/- 28.2 min). The stage of remission was negatively correlated with the 24-h mean and the mean peak amplitude of PRL. No patient showed a normal organization of sleep stages. On visual analysis there was no apparent association between EEG patterns and hormonal parameters. These results suggest that the endocrine hypothalamus is essentially intact in the chronic vegetative state. The observed changes may be due to an altered input from extrahypothalamic brain structures.

Adolescent↗
PubMed1989

[Long-term efficacy and side effect profile of a low-dose bemetizid-triamterene combination in patients with essential hypertension].

As only few data are available on the antihypertensive effectiveness and pattern of adverse reactions to low-dose diuretic treatment, a multicenter study was designed in which 77 patients with essential hypertension (WHO grades I to II) were followed up for one year with a view to answering the above questions. In patients who, at the end of a two weeks' placebo period had diastolic pressure values of more than 90 mmHg treatment was initiated with one daily tablet of a new preparation containing 10 mg bemetizide and 20 mg triamterene, for eight weeks. If, at the end of this interval, the target pressure values of less than 90 mmHg had not been attained, the dose was doubled. Blood pressure measurements (in sitting position) were repeated fortnightly, serum electrolytes, metabolic parameters and urinary triamterene fluorescence determined every four weeks. 56 of the 77 patients stayed on 10/20 mg bemetizide-triamterene for twelve months running. In 13 cases the dose had to be raised. Eight patients dropped out of the study. Average blood pressure values of 56 patients decreased from 169/103 mmHg (at the end of the placebo period) to 145/83 mm Hg after 52 weeks. Diastolic pressure reductions averaged 18 mmHg in 27 patients below the age of 49, 19 mmHg in 22 patients aged between 50 and 65, and 22 mmHg in seven patients older than 65 years. At the end of the 52 weeks' therapy, total serum cholesterol, HDL and LDL cholesterol, triglycerides, glucose and uric acid were unchanged in comparison to the placebo period in the entire group.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzothiadiazines↗
PubMed1989

[Treatment of hypertension in the aged].

Previous studies carried out on the treatment of hypertension in the elderly patient indicate that, in this group of patients, antihypertensive treatment can reduce cardiovascular mortality mainly by reducing mortality from cerebrovascular diseases. To date, the success of hypertensive treatment in over-80-year-olds with uncomplicated hypertension, and patients with isolated systolic hypertension, has not been documented. In the treatment of the elderly patient, age-specific pathophysiological changes need to be taken into account. Such changes are deteriorating renal performance, increased vasoconstriction, decreasing baroreceptor function, declining cardiac performance, and changes in the autoregulation of cerebral blood flow. For this reason, in geriatric hypertensives, the blood pressure should be reduced gradually over a period of weeks. Antihypertensive drugs with a natriuretic or vasodilative effect are pathophysiologically meaningful, while substances that result in a loss of potassium, depression of the sympathetic nervous system and negative inotropism are not so favorable.

Aged↗
PubMed1989

Increased forskolin stimulation of lymphocyte-adenylate cyclase in normotensive subjects predisposed to essential hypertension.

Since a significant heritability has been shown for forskolin stimulation of lymphocyte adenylate cyclase activity in twins, we evaluated lymphocyte forskolin-stimulated adenylate cyclase activity with respect to a familial predisposition towards essential hypertension. Lymphocyte adenylate cyclase activity was measured in broken cell preparations of 32 male normotensive volunteers with (n = 15) and without (n = 17) a positive family history of hypertension. The maximal forskolin stimulation of adenylate cyclase activity was significantly higher in the positive compared with the negative group (maximal stimulation of activity 53.5 +/- 3.4 versus 41.2 +/- 1.9 pmol cyclic AMP (cAMP)/mg protein per min; P less than 0.01). Dose-response curves showed a significantly greater stimulation of adenylate cyclase activity in the positive group at forskolin concentrations of 10(-7) to 2 x 10(-4) mol/l. The median effective dose (ED50) and adenylate cyclase activity in the absence of forskolin were similar in both groups. We conclude that lymphocyte forskolin-stimulated adenylate cyclase activity may depend in part on hereditary factors associated with a familial predisposition to essential hypertension.

Adenylyl Cyclases↗
PubMed1989

Alpha 2- and beta 2-adrenoceptor downregulation in marathon runners.

The regulation of platelet alpha 2- and lymphocyte beta 2-adrenoceptor densities by alterations in endogenous catecholamines was examined. In order to activate the sympathetic nervous system eight trained male normotensive subjects carried out a marathon run. Adrenoceptor densities and plasma catecholamine concentrations were measured before and immediately after the run. Platelet alpha 2-adrenoceptor density and lymphocyte beta-adrenoceptor density decreased after the run (P less than 0.05), whereas both plasma noradrenaline and adrenaline concentrations increased (P less than 0.01). Mean arterial pressure decreased (P less than 0.05), and the heart rate increased (P less than 0.001). The data suggest that increases in endogenous catecholamine concentrations cause downregulation of both alpha- and beta-adrenoceptor densities on human blood cells.

Adult↗
PubMed1988

Different effects of furosemide on alpha-adrenoceptors and on platelet aggregation in man.

The effect of a long-term administration of furosemide (2 x 30 mg/day for 3 weeks) on platelet alpha 2-adrenoceptor density and the fraction of high-affinity binding sites, as well as on platelet aggregation induced by adrenaline and ADP, was studied ex vivo in 8 normotensive volunteers. For comparison the in vitro effect of furosemide on platelet aggregation was also evaluated. Furosemide decreased alpha 2-adrenoceptor-density (P less than 0.01) and the fraction of high-affinity binding sites (P less than 0.05). Adrenaline-induced platelet aggregation was not altered ex vivo and in vitro. Furosemide inhibited ADP-induced platelet aggregation ex vivo (P less than 0.05) and in parallel in vitro (P less than 0.01) in a dose-dependent manner. The reduction of the density of alpha 2-adrenoceptors in the high affinity state may be of functional importance for the hemodynamic effects of furosemide. The inhibitory effect of furosemide on ADP-induced platelet aggregation ex vivo and in vitro, which is not related to the effects on adrenoceptors, seems to involve direct effects of furosemide on platelet function. It remains to be seen whether the latter effect is of clinical importance.

Adult↗
PubMed1987

Effects of nitrendipine and tiapamil on 45Ca2+ influx and on platelet aggregation.

The effects of the dihydropyridine derivative nitrendipine and of the phenylalkylamine derivative tiapamil on 45Ca2+ influx was determined in platelets in vitro and on platelet aggregation ex vivo. Thrombin-stimulated 45Ca2+ influx was inhibited by 10 mumol/l nitrendipine and 100 mumol/l tiapamil. ADP- and adrenaline-induced platelet aggregation were inhibited in normotensive volunteers following short-term administration of nitrendipine (20 mg b.i.d.) but not after tiapamil (225 mg t.i.d.). Therefore, mechanisms other than the inhibition of Ca2+ influx should be considered to be responsible for inhibition of platelet aggregation by nitrendipine ex vivo.

Adult↗
PubMed1987

Regulation of alpha 2-adrenoceptor density in normotensive and hypertensive man.

We examined normotensive and hypertensive subjects in order to determine whether changes in platelet alpha 2-adrenoceptor density following alterations in plasma noradrenaline are related to changes in noradrenaline (NA) reactivity. Noradrenaline reactivity, plasma NA, alpha 2-adrenoceptor density, and adenylate cyclase activity were measured before and after a 24-h infusion of NA at a subpressor dose (0.02 micrograms/kg per min, n = 13), and also after application of drugs known to increase (nifedipine and furosemide) or decrease (clonidine) plasma NA. Measurements were obtained 60 min after nifedipine (20 mg in a single dose, n = 13), after 3 weeks on furosemide (30 mg twice a day, n = 8) and after 1 week on clonidine (150 micrograms three times a day, n = 5). Infusion of NA decreased alpha 2-adrenoceptor density (P less than 0.01) and NA reactivity (P less than 0.05). Nifedipine decreased alpha 2-adrenoceptor density and NA reactivity (P less than 0.01 for both) in patients with essential hypertension. The alterations in alpha 2-adrenoceptor densities were paralleled by a decreased adrenaline-induced inhibition of adenylate cyclase activity (P less than 0.01). Furosemide decreased alpha 2-adrenoceptor density (P less than 0.01), the fraction of high-affinity binding sites (P less than 0.01) and NA reactivity (P less than 0.05) in normotensive subjects. Following clonidine all three parameters, alpha 2-adrenoceptor density, the fraction of high affinity sites and NA reactivity, increased (P less than 0.05 for each).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1986

[Cerebral hemodynamics in chronic hypoxic hypoxia].

The effects of chronic-hypoxic hypoxia on cerebral blood flow and its regulating mechanisms were investigated by means of intracardiac injection of radioactively labelled microspheres. In a gas chamber designed and constructed for the purpose, adult cats were exposed to stepwise decreasing inspiratory oxygen concentrations (for 4.5 months with a final O2 concentration of 8 vol%). Using animals adapted to hypoxic hypoxia, responsiveness of cerebral blood flow either to alterations in systemic arterial pressure (SAP) or to alterations in arterial blood oxygen tension (PaO2) were assessed. Flow measurement was done under three different conditions: normoxic normotension (PaO2 greater than 100 mmHg; SAP greater than 100 mmHg), hypoxic normotension (PaO2 = 30 mmHg; SAP greater than 100 mmHg), or normoxic hypotension (PaO2 greater than 100 mmHg; SAP = 60 mmHg). Hematocrit values continuously increased to 56% during the process of adaptation to hypoxia. There was also a remarkable increase in cardiac output of hypoxia-adapted animals subjected to hypoxia and to normoxia. Chronic-hypoxic hypoxia led to increased cerebral blood flow, which persisted even when animals were returned to normoxia. Under hemorrhagic hypotension, cerebral blood flow fell significantly in animals adapted to chronic-hypoxic hypoxia but did not fall short of the absolute values in controls. The relative reduction in cerebral blood flow might be attributable to the decrease in cardiac output and to altered blood viscosity. This implied that, even in animals subjected to long-standing graded hypoxic hypoxia, autoregulatory capacity might be partly preserved.

Adaptation, Physiological↗