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Biomedical subjects

W Zidek

Publications and source records attributed to W Zidek.

At least 235 records · Page 13Linked to original sources
PubMed1989

Transmission of hypertension in rats by cross circulation.

Cross circulation was performed in 54 couples of spontaneously hypertensive and normotensive rats. Blood was pumped through two anastomoses between the carotid arteries and external jugular veins in both directions with equal flow rate. In normotensive rats cross-circulated with untreated spontaneously hypertensive rats mean arterial pressure increased by 20.9 +/- 12.2 mm Hg (p less than 0.01). Administration of digoxin antibody in a dose binding 0.25 mg digoxin to the spontaneously hypertensive rats before cross circulation prevented the transmission of hypertension to the normotensive rat, whereas chemical sympathectomy with 6-hydroxydopamine and intravenous injection of inactive Fab fragments had no inhibitory effect. It is concluded that, in this strain of spontaneously hypertensive rats, a circulating hypertensive factor exists. The factor binds to digoxin antibody and is not produced in sympathetic nervous tissue.

Animals↗
PubMed1989

Evaluation of the therapeutic effect of transdermal beta-blocker therapy in patients with essential hypertension.

Transdermal drug delivery has been applied to various agents in an effort to decrease the frequency of drug administration and improvement of the patients compliance. In the present study, it could be demonstrated that transdermal monotherapy (BIO TSD) with a beta-blocker (20 mg mepindolol) in patients with essential hypertension led to an effective 24 h blood pressure lowering effect within 1 week (160.1 +/- 6.1 mmHg/95.8 +/- 8.3 mmHg vs. 136.8 +/- 7.2 mmHg/84.3 +/- 5.0 mmHg; p less than 0.05). Also a reduction of excessive blood pressure peaks in the circadian blood pressure profiles was observed. Studies comparing transdermal with oral beta-blocker administration in hypertensive patients would further substantiate the value of this new therapeutic system as an antihypertensive treatment.

Administration, Cutaneous↗
PubMed1989

[Cellular electrolyte metabolism and regulation of vascular tonus. Clinical aspects].

In the pathogenesis of essential hypertension the role of intracellular Na+ concentrations due to the secretion of a yet unidentified natriuretic factor is being discussed. Proceeding from the role of Ca++ in vascular smooth muscle contraction the hypothesis of increased intracellular free Ca++ concentrations in essential hypertension has been proposed. The measurements described here first revealed increased cellular concentrations of free Ca++ in essential hypertensives. Furthermore in essential hypertensives and in the spontaneously hypertensive rat a circulating factor was demonstrated increasing blood pressure and stimulating cellular Ca++ uptake.

Animals↗
PubMed1988

Age-dependent increase in arterial smooth muscle calcium in spontaneously hypertensive rats.

Alterations in cellular calcium metabolism in essential hypertensive and in the SHR have been described. In the present study, particle-induced X-ray emission (PIXE) was used to get some information on the spatial distribution of Ca2+ in aortas of spontaneously hypertensive rats (SHR) and normotensive controls aged 1 week, 4 weeks, and 12 weeks. It was found that the Ca2+ content was not elevated in the aortic smooth muscle of SHR aged 1 week (n = 9) as compared to normotensive controls (n = 8) (186.8 +/- 89.9 micrograms Ca2+/g tissue vs 254.0 +/- 73.7 micrograms Ca2+/g tissue. The Ca2+ content was significantly raised in the aortic smooth muscle of SHR aged 4 weeks (n = 9) as compared to 4-weeks-old WKY rats (n = 12) (726.0 +/- 130.4 Ca2+/g tissue vs 440.3 +/- 214.4 Ca2+ micrograms/g tissue and in SHR aged 3 months (n = 15) as compared to WKY rats (n = 12), respectively (3317.0 +/- 734.0 micrograms Ca2+/g tissue vs. 1632.0 +/- 569.6 micrograms Ca2+/g tissue). The results confirm the age-related increase in the arterial Ca2+ content in normotensive rats and demonstrate additionally that this age-related rise in arterial Ca2+ content is accelerated in SHR.

Aging↗
PubMed1988

Effect of hypertensive plasma on Ca2+ transport in human neutrophils.

The effects of plasma fractions from essential hypertensives (n = 17) and normotensives (n = 17) on Ca2+ transport in permeabilised human neutrophils were studied using an ion-selective electrode. The plasma fractions were obtained by gel filtration and contained substances with a molecular weight in the range of 1000-1500 Da. When isolated from essential hypertensives, this fraction had been shown to increase blood pressure after intravenous injection in the rat. The rate of Ca2+ uptake by permeabilised neutrophils after addition of extracellular Ca2+ was significantly accelerated during incubation of the cells with the hypertensive fraction (855.9 +/- 812.3% vs 218.0 +/- 294.3% of the control value, P less than 0.05). In a suspension with intact neutrophils hypertensive plasma fractions (n = 7) caused an increase of extracellular pCa by 0.479 +/- 0.115 (P less than 0.01), whereas the normotensive fractions did not change pCa significantly. It is concluded that the hypertensive plasma fraction increases Ca2+ accumulation in subcellular particles. Additionally the Ca2+ influx through the plasma membrane is increased by the circulating hypertensive factor.

Adult↗
PubMed1988

Effect of plasma from hypertensive subjects on Ca2+ transport in permeabilized human neutrophils.

1. The effects of plasma fractions from essential hypertensive subjects (n = 14) and normotensive subjects (n = 14) on Ca2+ transport in permeabilized human neutrophils was studied using an ion-selective electrode. 2. Plasma fractions were obtained by gel filtration and contained substances with a molecular mass in the range 1000-1500 daltons. This fraction isolated from essential hypertensive subjects has been shown to increase blood pressure after intravenous injection in the rat. 3. The rate of Ca2+ uptake by permeabilized neutrophils after addition of extracellular Ca2+ was significantly accelerated during incubation of the cells with the hypertensive fraction (1049.3 +/- 807.7% vs 242.5 +/- 320.9% of the control value, mean +/- SD, P less than 0.05). 4. It is concluded that the hypertensive plasma fraction increases Ca2+ accumulation in subcellular particles, so that under excitatory conditions Ca2+ release in arterial smooth muscle might be enhanced.

Adult↗
PubMed1988

Transdermal beta-blocker therapy in essential hypertension.

Transdermal drug delivery has been applied to various agents in an effort to decrease the frequency of drug administration and increase the patients compliance. In our study, we demonstrated that transdermal application of a beta-blocker (20 mg mepindolol) in patients with essential hypertension led to effective blood pressure lowering effect within 1 week (160.1 +/- 6.1 mm Hg/95.8 +/- 8.3 mm Hg vs 136.8 +/- 7.2 mm Hg/84.3 +/- 5.0 mm Hg; P less than 0.05). A controlled study of transdermal versus oral beta-blocker administration in hypertensives is necessary before this new therapeutic system is introduced in antihypertensive treatment.

Administration, Cutaneous↗
PubMed1988

Effect on blood pressure of chemically induced renomedullectomy in normotensive and spontaneously hypertensive rats.

An antihypertensive function in systemic blood pressure control has been attributed to the renal medulla. In order to examine this hypothesis normotensive and spontaneously hypertensive rats of the Münster strain (SHR) were chemically renomedullectomized by 2-bromoethylamine hydrobromide (BEA), injected intraperitoneally in a single dose of 200 mg/kg body weight. Within 5 weeks blood pressure of the BEA-treated normotensive rats and SHR rose by 17.2 +/- 15.2 and 27.7 +/- 21.0 mmHg (mean values +/- s.d; P less than 0.01), respectively, returning to baseline after 2 further weeks. Blood pressure was unchanged in the normotensive rats and SHR controls that were given isotonic saline instead of BEA solution. During maximum blood pressure in BEA-treated animals histological signs of severe renomedullary inflammation with papillary necrosis were demonstrable, while urine flow rates were elevated. Despite these disturbances renal function remained normal. These similar responses make it unlikely that a lack of a renomedullary vasodilator plays a major role in the pathogenesis of spontaneous hypertension in the Münster strain.

Animals↗
PubMed1988

Analysis of Ca2+ in aortic tissue: age-dependent Ca2+ content in spontaneously hypertensive rats and in normotensive controls.

In the present study particle-induced X-ray emission (PIXE) was used to analyse the spatial distribution of Ca2+ in aortic tissue of spontaneously hypertensive rats (SHR) and normotensive controls aged 1 week, 4 weeks and 12 weeks. Ca2+ was not elevated in the aortic smooth muscle of SHR aged 1 week (n = 9) compared with normotensive controls (n = 8; 186.8 +/- 89.9 micrograms Ca2+/g tissue). Ca2+ was significantly increased in the aortic smooth muscle of SHR aged 4 weeks (n = 9) compared with 4-week-old Wistar-Kyoto (WKY) rats (n = 12; 726.0 +/- 130.4 micrograms Ca2+/g tissue versus 440.3 +/- 214.4 micrograms Ca2+/g tissue) and in SHR aged 3 months (n = 15) compared with WKY (n = 12), (3317.0 +/- 734.0 tissue versus 1632.0 +/- 569.6 micrograms Ca2+/g tissue, respectively). The results confirm an age-related increase in arterial Ca2+ in normotensive rats and demonstrate that this age-related rise is accelerated in SHR.

Animals↗
PubMed1988

Assessment of intracellular sodium and calcium in essential hypertension during diuretic treatment.

In 87 essential hypertensive patients, torasemide (1- isopropyl-3-([4-(3-methyl-phenylalmino)pyridine]-3-sulfonyl)urea), a new long-acting high-ceiling diuretic, was applied for 6 months in order to assess its effects on blood pressure and intracellular electrolytes. In a randomized trial 42 patients received 2.5 mg and 45 patients 5 mg torasemide once daily. In all patients, diastolic blood pressure was greater than 100 mm Hg before treatment. Blood pressure normalisation (diastolic blood pressure greater than or equal to 90 mmHg) was observed in 21 out of 42 patients receiving 2.5 mg torasemide daily and in 26 out of 42 patients with 5 mg torasemide throughout the study. In both groups doubling of the dosage was performed in these patients who had an insufficient blood pressure control after 4 weeks. In the majority of these non-responders blood pressure normalisation was achieved during the higher dosages. In the total group of patients there was an elevation of the intracellular sodium and a decrease of the intracellular calcium, measured with the ion-selective electrode in red blood cells. It could be shown that the decrease in blood pressure induced by torasemide was accompanied by a decrease of intracellular Ca2+, thus supporting the hypothesis that intracellular free Ca2+ is an important regulator of vascular tone in essential hypertension.

Adult↗
PubMed1987

[Computer-assisted assessment of the 24-hour blood pressure profile in essential and secondary hypertensive patients].

In 17 essential hypertensives, 13 secondary hypertensives and 9 normotensives, noninvasive 24 h blood pressure monitoring was performed. By a computer-aided evaluation according to the Cosinor method, circadian periodicity was quantified and expressed as a coefficient of periodicity in %. This coefficient for systolic pressure was higher in essential hypertensives and normotensives than in secondary hypertensives (42.9 +/- 18.0 et 43.0 +/- 16.7 versus 28.2 +/- 17.7; p less than 0.05). The circadian periodicity of diastolic pressure showed no significant differences. Despite the large overlap, coefficients of periodicity below 20% for systolic pressure may suggest secondary hypertension.

Adult↗
PubMed1987

Cellular calcium metabolism in primary hypertension.

Several disturbances of cellular Ca2+ metabolism have been described in essential hypertension and in the spontaneously hypertensive rat. Possibly the elevation of intracellular free Ca2+ concentration in arterial smooth muscle cells is one important step in the pathogenesis of primary hypertension. In most studies a decreased energy-dependent Ca2+ transport has been proposed as a mechanism. However, disturbances in cellular Ca2+ metabolism, which can be exclusively ascribed to essential hypertension, have not yet been found. The cause of altered cellular Ca2+ transport in primary hypertension may either be a genetically determined defect of membrane transport or a still-unidentified humoral factor.

Animals↗
PubMed1987

Calcium and primary hypertension.

The role of dietary calcium in essential hypertension remains controversial. Various studies have found on the one hand a weak negative correlation between blood pressure and Ca2+ intake in special groups, and on the other hand a positive correlation between serum Ca2+ concentration and blood pressure. Several disturbances of cellular Ca2+ metabolism have been described in essential hypertension and in the spontaneously hypertensive rat. Possibly the elevation of intracellular free Ca2+ concentration in arterial smooth muscle cells is one important step in the pathogenesis of primary hypertension. In most studies a decreased energy-dependent Ca2+ transport has been proposed as a mechanism. However, disturbances in cellular Ca2+ metabolism, which can be exclusively ascribed to essential hypertension, have not yet been found. The cause of altered cellular Ca2+ transport in primary hypertension may either be a genetically determined defect of membrane transport or a still unidentified humoral factor.

Animals↗
PubMed1987

Cadmium and hypertension.

Cadmium, an environmental trace metal, has been implicated as a possible factor in human hypertension. Although the epidemiological studies on humans exposed to cadmium are biased by certain additional factors, more detailed information is available from animal studies and in vitro experiments. The results demonstrate that cadmium influences the vasopressor-induced reactivity and the stress strain characteristics of the blood vessel wall. Thus, it is conceivable that cadmium might contribute to the elevation of blood pressure. But still more convincing data are necessary to clarify the link between cadmium exposure and the development of human hypertension.

Animals↗
PubMed1987

A circulating hypertensive factor in primary hypertension: effect of antihypertensive therapy.

In this study the role of a humoral hypertensive factor in spontaneously hypertensive rats (SHR) of the Münster strain was examined by cross-circulation. It was demonstrated that hypertension of the SHR could be transmitted to cross-circulation normotensive Wistar-Kyoto rats. The results led to the following conclusion: primary hypertension is caused by a circulating factor which is produced by kidneys and adrenals and suppressed by acute volume depletion and chronic dietary salt restriction. The antihypertensive effect of nifedipine probably leads to a compensatory stimulation of the hypertensive factor in SHR.

Adrenalectomy↗
PubMed1987

Intracellular calcium in secondary hypertension.

In 13 essential hypertensives, 15 renal hypertensives, 16 patients with phaeochromocytoma, 6 patients with renal artery stenosis and in 21 normotensive controls the Ca2+ and K+ content in the asked material from red blood cells was determined by flame photometry. Furthermore, intracellular K+ concentration was measured in the haemolysate. The ratio between Ca2+ and K+ concentration in ashed red blood cells (Cai2+/Ki+) was 2.07 +/- 0.9110-3 in normotensives, 4.58 +/- 1.68 10(-3) in essential hypertensives (p less than 0.01), 3.13 +/- 1.90 10(-3) in renal hypertensives (p less than 0.05), 2.15 +/- 1.62 in patients with phaeochromocytoma and in patients with renal artery stenosis 2.25 +/- 1.25. Intracellular K+ concentration was 94.3 +/- 3.1 mumol/l in normotensives, 94.7 +/- 3.8 mumol/l in essential hypertensives and 93.8 +/- 3.9 mumol/l in renal hypertensives, 198.2 +/- 149.1 mumol/l in patients with phaeochromocytoma and 201.1 +/- 139.1 mumol/l in patients with renal artery stenosis. Therefore, intracellular total Ca2+ concentrations is concluded to be increased in red blood cells from essential hypertensives and, to a lesser extent, in those from renal hypertensives. The method to determined Cai2+/Ki+ in the red blood cells may thus be suitable to assess cellular Ca2+ content in hypertension.

Adrenal Gland Neoplasms↗