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Biomedical subjects

W Zidek

Publications and source records attributed to W Zidek.

At least 253 records · Page 14Linked to original sources
PubMed1987

The effect of antihypertensive treatment on the circulating hypertensive factor in the spontaneously hypertensive rat.

To elucidate the role of circulating hypertensive factors in the spontaneously hypertensive rat and the effects of antihypertensive treatment on the circulating hypertensive factor, cross circulation was performed in 54 couples of spontaneously hypertensive and normotensive rats. 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). Increases in mean arterial pressure were also obtained by cross-circulation with spontaneously hypertensive rats pretreated with propranolol, furosemide, and nifedipine. Mean arterial pressure was not changed by cross circulation after pretreatment of the spontaneously hypertensive rats with alpha methyldopa. It is concluded that in this strain of spontaneously hypertensive rats a circulating hypertensive factor exists, the secretion of which can be suppressed by the centrally acting drug, alpha methyldopa. Therefore either the central nervous system may take part in the regulation of the factor or the factor may be synthetized in the central nervous system.

Animals↗
PubMed1987

Arterial resistance vessels in primary hypertension--evidence for altered cellular Ca2+ metabolism.

The role of intracellular free Ca2+ in arterial smooth muscle was investigated in aortic smooth muscle cells from spontaneously hypertensive and normotensive rats, as well as in porcine aortic smooth muscle. Intracellular free Ca2+ in aortic smooth muscle from spontaneously hypertensive rats was elevated. Incubation of porcine aortic smooth muscle with plasma from essential hypertensive and normotensive subjects revealed a humoral factor in subjects with essential hypertension, which increased intracellular free Ca2+. Cross-circulation experiments between spontaneously hypertensive and normotensive rats demonstrated a transmission of hypertension to the normotensive animals as a result of a circulating hypertensive factor possibly produced in the kidneys and adrenals. The experiments suggest that vasoconstriction in primary hypertension may be caused by a humoral factor that increases intracellular free Ca2+ in arterial smooth muscle.

Animals↗
PubMed1987

Humoral vasopressor agents in primary hypertension.

In essential hypertension and in the spontaneously hypertensive rat, there are indications for a yet unidentified vasopressor agent which may play an important role in pathogenesis. It has been demonstrated in the spontaneously hypertensive rat by parabiosis, cross-circulation, cross-transplantation of kidneys and by injection of hypertensive plasma fractions. In plasma from essential hypertensives, an agent sensitizing the vasculature to pressor hormones and a substance with direct vasopressor actions have been found. The relationship of the hypertensive factor to the natriuretic hormone is not clear.

Animals↗
PubMed1987

[Relations between the cortical DC potentials and the K+ concentration of the blood and cerebral cortex extracellular space in reversible asphyxia].

The relationship between changes of the cortical DC potential and the K+ concentration gradient across the blood-brain barrier (BBB) was studied in the rat brain during short ventilatory arrest. For this purpose K+ concentrations were measured simultaneously in the extracellular space of the cerebral cortex and in the streaming blood of the carotid artery and the superior sagittal sinus. For measurements ion-selective micro- and macro-electrodes based on the K+ ionophore valinomycin were used. During reversible asphyxia free K+ concentrations in the circulating blood and in the extracellular fluid of the brain tissue increased and re-decreased with different time courses. The resulting difference between the electromotive forces of the ion-selective signals resembled the course of the cortical DC potential during the initial phase of the ventilatory arrest during the post-asphyxiation period. The results suggest that during these events the cortical tissue including the BBB behaves like a K+-selective membrane which is probably located at the blood-brain interface. It is concluded that the capillary-glial complex may principally contribute to the generation of DC shifts associated with the asphyxiation process.

Animals↗
PubMed1987

Effects of drugs on magnesium requirements.

A number of drugs can influence Mg metabolism and produce changes in serum Mg concentrations. These alterations must always be considered in the differential diagnosis of cases with Mg disturbances. Hypermagnesemia is seen, particularly after administration of Mg-containing drugs in renal insufficiency. Marked hypomagnesemia can be observed in a great number of patients, particularly in those treated with loop diuretics, osmotic substances and with antineoplastics, such as cisplatin.

Anti-Bacterial Agents↗
PubMed1986

Weight reduction and salt restriction in hypertension: effects on blood pressure and intracellular electrolytes.

In 16 essential hypertensives on a program of energy restriction (800 kcal/day) with and without simultaneous salt restriction, the effects on blood pressure and intracellular Na+ and Ca2+ in red blood cells were studied. A decrease in blood pressure and intracellular free Na+ and Ca2+ was only observed in the cases of simultaneous energy and salt restriction. The beneficial effect of weight reduction in hypertension thus depends on a diminished salt intake and is probably mediated by changes in intracellular free Ca2+.

Adult↗
PubMed1986

What's new in cellular cation exchange and humoral factors in primary hypertension?

In essential hypertension abnormalities of cellular Na+ and Ca++ handling have been described. The latter disturbance probably offers an explanation for the increased vasoconstriction in essential hypertension. The etiology of those disturbances in cellular Na+ and Ca++ metabolism may be related to genetic disturbances of membrane transport, or to a humoral factor influencing cellular cation metabolism.

Calcium↗
PubMed1986

Ca2+i:K+i ratio and total intracellular calcium in essential and renal hypertension.

The calcium ion (Ca2+) and potassium ion (K+) content in the ashed material from red blood cells was determined by flame photometry in 61 essential hypertensives, 11 renal hypertensives and in 47 normotensive controls, and intracellular K+ concentration was measured in the haemolysate. The ratio between Ca2+ and K+ content in ashed red blood cells (Ca2+i:K+i) was 2.07 +/- 0.91 X 10(-3) in normotensives, 4.91 +/- 2.17 X 10(-3) in essential hypertensives (P less than 0.01) and 3.48 +/- 2.04 X 10(-3) in renal hypertensives (P less than 0.05). Intracellular K+ concentration was 94.3 +/- 3.1 mmol/l in normotensives, 94.7 +/- 3.8 mmol/l in essential hypertensives and 93.8 +/- 3.9 mmol/l in renal hypertensives. Therefore intracellular total Ca2+ concentration is increased in the red blood cells from essential hypertensives and, to a lesser extent, in the red blood cells from renal hypertensives. The use of Ca2+i:K+i ratios in red blood cells may thus be useful in assessing cellular Ca2+ content in hypertension.

Adult↗
PubMed1986

Effects on blood pressure of cross circulation between spontaneously hypertensive and normotensive rats.

In order to examine the role of humoral factors for the development of hypertension in the spontaneously hypertensive rat of the Münster strain (SHR) cross circulation experiments with normotensive Wistar Kyoto rats were performed. Cross circulation between SHR and normotensive rats for 30 min increased mean arterial pressure in the latter by 29.1 +/- 7.6 mm Hg (p less than 0.01). Transmission of hypertension by cross circulation was abolished by nephrectomy, adrenalectomy, volume depletion or chronic salt restriction in the SHR. It is concluded that hypertension in SHR is caused by a circulating hypertensive agent produced in kidneys and adrenals, the secretion of which can be suppressed by volume or salt depletion.

Adrenalectomy↗
PubMed1986

Elemental and trace element distribution in medical samples: analysis by proton-induced X-ray emission.

The analysis of trace elements is performed by proton-induced X-ray emission. The process is most effective if the velocity of the exciting particles--protons--is similar to the velocity of the electron on its orbit in the simple atomic model of Bohr. For K-shell electrons of the elements with 15 less than or equal to z less than or equal to 40 this requires proton energies of a few MeV, available from electrostatic van de Graaf accelerator machines. After knocking out the K-shell electron, the empty place is filled up by electrons jumping from higher orbits with simultaneous emission of characteristic X-rays, which are registered with a cooled Si (Li) detector. By a set of electrodes the beam can be swept across the specimen surface. Therefore this method yields an excellent correlation of trace element distribution within the morphological structure of organic tissue. In the present study the sweep went along a line perpendicular to the arterial wall layers (aortic, renal artery and heart muscle) of normotensive and spontaneously hypertensive rats. Along this line all elements and trace elements are recorded simultaneously. These are P, S, Cl, K, Ca, Fe, Cu, Zn, Br and Sr. The trace element content of the aortic wall and the renal artery, of 22 spontaneously hypertensive and 11 normotensive rats and of human heart muscle was investigated. The results demonstrate that Zn was only detected in the muscle-containing layers of the arteries. There was no different distribution between hypertensive and normotensive rats. However, Ca2+ was mainly detected in the smooth muscle-containing tunica media of hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Ca2+ metabolism in arteries of spontaneously hypertensive rats: assessment by proton-induced X-ray emission.

Changes of intracellular Ca2+-metabolism have been considered to be of importance for the pathogenesis of essential hypertension. In the present study particle-induced X-ray emission (PIXE) was used to get information on the spatial distribution of Ca2+ in aortas and renal arteries of spontaneously hypertensive (SHR) and normotensive rats. Our findings demonstrate a significant Ca2+ elevation in the aorta and renal artery of SHR versus normotensive Wistar-Kyoto (WKY) rats (3317 +/- 734 micrograms Ca2+/g tissue versus 1623 +/- 569 micrograms Ca2+/g tissue and 3432 +/- 1867 micrograms Ca2+/g tissue versus 1050 +/- 554 micrograms Ca2+/g tissue).

Animals↗
PubMed1985

Treatment of resistant hypertension by phlebotomy.

In 15 essential hypertensives resistant against a standard triple combination of antihypertensive drugs phlebotomy was performed. Mean arterial pressure was lowered from 140.1 +/- 12.2 mm Hg to 123.8 +/- 14.9 mm Hg after 14 days. No serious side effects were observed. The duration of the hypotensive effect of phlebotomy was about 4 weeks. Phlebotomy can be used in addition to drug treatment in resistant essential hypertension.

Adult↗
PubMed1985

[Leg edema].

Explore the source record for details and available documents.

Adult↗
PubMed1985

Intracellular chloride in essential hypertension.

In 25 patients with untreated essential hypertension and 25 healthy controls, erythrocyte intracellular Cl- concentration and activity as well as Na+ activity were measured. Intracellular Cl- concentration in essential hypertensive patients was 70.6 +/- 11.3 as compared with 84.4 +/- 9.5 mmol/l in the controls (P less than 0.001). Intracellular Cl- activity was 77.5 +/- 13.0 mmol/l of cell water in hypertensive patients, the control value being 100.8 +/- 11.0 mmol/l of cell water (P less than 0.001). In the hypertensive group intracellular Na+ activity was 14.3 +/- 4.1 as compared with 7.1 +/- 1.8 mmol/l of cell water in the normotensive group (P less than 0.01). From these results it is suggested that in essential hypertension not only disturbances of cation metabolism, but also of anion metabolism, occur. Possibly the Cl- changes reflect a decreased Cl- inward transport due to an altered Na-K cotransport.

Adult↗