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Biomedical subjects

W Zidek

Publications and source records attributed to W Zidek.

At least 307 records · Page 17Linked to original sources
PubMed1982

Intracellular Na+ and Ca2+ activities in aortic smooth muscle cells from spontaneously hypertensive rats.

Elevations of intracellular Na+ and Ca2+ in essential hypertension have up to now only been demonstrated in blood cells. Therefore, intracellular Na+ and Ca2+ activities were determined in cultured aortic smooth muscle cells from nine spontaneously hypertensive rats of the Münster strain and from nine normotensive Wistar rats. Intracellular ion activities were determined by ion-selective electrodes. In muscle cells from spontaneously hypertensive rats intracellular Na+ activity was markedly elevated (P less than 0.01), whereas intracellular Ca2+ was not significantly different. This points to the preponderance of genetic causes for the elevation of intracellular Na+, whereas the disturbances in cellular Ca2+ metabolism may additionally require humoral factors to become manifest.

Animals↗
PubMed1982

Effect of nifedipine on blood pressure and on intracellular calcium in arterial hypertension.

In 13 patients with essential and renal hypertension, the influence of nifedipine on the intracellular free Ca2+ concentration was tested. Measurements of free Ca2+ were performed with a Ca2+ -selective electrode. The patients were additionally treated with a conventional antihypertensive combination therapy, by which the blood pressure could not be lowered satisfactorily. Under treatment with 30-60 mg of nifedipine daily, blood pressure was lowered from 192 +/- 23/95 +/- 15 mm Hg to 147 +/- 20/83 +/- 16 mm Hg. The intracellular Ca2+ activity fell from 7,115 +/- 14,139 to 1,886 +/- 3,748 mumol/L (p less than 0.05). The decrease in intracellular Ca2+ correlated very well with the initial value of Ca2+ activity (r = 0.966); furthermore, a relationship was found with the serum creatinine level (r = 0.48). On the other hand, there was no correlation with the decrease in blood pressure. In the lower dose range, nifedipine did not elicit a clear reduction in intracellular Ca2+. The results show that intracellular Ca2+ activity can be influenced by Ca2+ antagonists, but that there is no direct relationship between intracellular free calcium and blood pressure.

Adult↗
PubMed1981

[Computerized tomography in adrenal diseases with excessive production of hormones].

In 41 patients with adrenal diseases and hormonal excess (pheochromocytoma n = 9, Cushing's syndrome n = 6, primary aldosteronism n = 26) computer tomography was performed for localization and classification of the adrenal lesion(s). In all patients diagnosis was confirmed by surgery. In all patients with pheochromocytoma a tumor was detected. 8 patients had unilateral adrenal pheochromocytoma, whereas in one female patient the pheochromocytoma was multilocular. 4 of the 6 patients with hypothalamic-pituitary Cushing's syndrome had enlargement of the adrenals. In the 26 patients with primary aldosteronism, computed tomography showed normal adrenal glands in 2 of the 17 patients with unilateral adenoma (with a diameter of 8 mm in both of the 2 patients) and in 6 of the 9 patients with bilateral hyperplasia. In the remaining patients adenoma or hyperplasia was detected. The results document that in patients with pheochromocytoma, with Cushing's syndrome, and in those with primary aldosteronism, computed tomography is a simple and valid method for localization and classification of the adrenal lesion(s). In primary aldosteronism with a normal adrenal computed tomography, however, differentiation between a small unilateral adrenal adenoma and bilateral adrenal hyperplasia remains problematic.

Adrenal Gland Neoplasms↗
PubMed1981

Zinc concentrations in plasma and erythrocytes in digitalized patients.

Determination of zinc, sodium, potassium and magnesium in plasma and red blood cells were performed in 31 controls and 63 patients treated with digitalis. In digitalized patients sodium and zinc concentrations in red blood cells were significantly increased. The intraerythrocyte magnesium and potassium levels as well as all investigated electrolytes in plasma remained within the normal range. There was a close relationship between the increase of sodium and zinc content in red blood cells, indicating alterations in transmembrane transport mechanisms induced by digitalis therapy.

Digitalis Glycosides↗
PubMed1981

[Intracellular sodium and calcium as a genetic marker in essential hypertension].

In 33 normotensive probands with a familial disposition to hypertension and in 18 normotensives without a family history of hypertension, aged 15 to 24 years, intracellular Na+ and Ca2+ activity in red blood cells was determined by ion-selective electrodes. The activities represent the free, i.e. unbound intracellular fraction of each ion. In the group with a family history of hypertension the mean intracellular Na+ activity was 9.74 +/- 1.43 mmol/l and clearly exceeded that in the group without predisposition to hypertension, which was 7.74 +/- 1.06 mmol/l. Even larger differences were found in mean intracellular Ca2+ activity (9.54 +/- 9.56 mumol/l in the group with familial disposition and 1.87 +/- 3.47 mumol/l in the control group). However, due to the relatively wide range of the values, especially with respect to the Ca2+ activities in probands with familial disposition to hypertension, the values from the two groups overlapped. The results suggest that elevation of intracellular Na+ and Ca2+ activity may be evidence for a genetically determined later development of hypertension.

Adolescent↗
PubMed1981

Intracellular cation activities and concentrations in spontaneously hypertensive and normotensive rats.

1. The intracellular concentrations of Na+,K+ and Ca2+ were measured in the erythrocytes of spontaneously hypertensive rats and normotensive Wistar rats. 2. The intracellular Na+ concentration in hypertensive rats was slightly elevated at 3.16 +/- 0.25 compared with 2.85 +/- 0.35 mmol/l (P approximately 0.05) and intracellular Na+ activity was markedly increased in hypertensive rats. 3. Intracellular Ca2+ activity was 7519 +/- 28990 nmol/l of free water in hypertensive rats compared with 123 +/- 98 in controls (P less than 0.01). 4. The cytoplasm of hypertensive animals did not buffer Ca2+ as effectively as that of normal animals. 5. It is concluded that a decreased binding capacity of intracellular macromolecules for Na+ and Ca2+ may explain the disturbances of intracellular electrolyte composition in spontaneously hypertensive rats.

Animals↗
PubMed1981

Intracellular Na+ as a genetic marker of essential hypertension.

In 1960 the pathophysiological mechanisms by which Na+ is involved in human essential hypertension were first elucidated by the finding that intracellular Na+ is elevated in red blood cells of essential hypertensives. Furthermore it was found that (1) transmembranous Na+ fluxes in red blood cells of essential hypertensives are changed in parallel with intracellular Na+ concentration, reflecting the metabolic disturbances better than the Na+ concentration measurements, (2) in normotensives with a familial disposition of essential hypertension intracellular Na+ and transmembranous Na+ fluxes are elevated, (3) uremia affects intracellular Na+ levels similarly as essential hypertension, and (4) intracellular free Na+ and free Ca++ is increased in spontaneously hypertensive rats. It can be assumed that elevated intracellular Na+ plays a causative role in essential hypertension.

Animals↗
PubMed1981

[Disturbed sodium and calcium exchange in erythrocytes of spontaneously hypertensive rats (author's transl)].

In red blood cells of spontaneously hypertensive and of normotensive rats intracellular NA+ activity (a(i)Na), Na+ concentration (]Na+]i) and Ca2+ activity (a(i)Ca) were measured by ion-selective electrodes and flame photometry, respectively. In spontaneously hypertensive rats a(i)Na and a(i)Ca were significantly elevated as compared with the normotensive controls, whereas [Na+]i showed no significant difference. In hypertensive animals a(i)Na, exceeded [Na+]i, in normotensive rats a(i)Na was lower than [Naf+]i. From these results it can be concluded: (1) In spontaneously hypertensive rats the transmembraneous distribution of free Na+ is altered, (2) an elevation of intracellular free Ca2+ may contribute to increased vascular contractility in hypertensive animals, (3) the described abnormalities may be caused by a lowered binding-capacity of intracellular macromolecules for Na+ and Ca2+.

Animals↗
PubMed1979

Temperature dependent membrane potential changes in snail neurons and their relation to active ion transport.

The mechanisms underlying the temperature response of the resting membrane potential (RMP) were investigated in 3 identified neurons of the buccal ganglion of Helix pomatia. Lowering the temperature evoked a decrease of the RMP and an increase in membrane resistance, and vice versa. The temperature response of the RMP had an equilibrium potential of ca, -60 mV. It is essentially evoked by changes in the potassium conductance. Indications of an electrogenic sodium transport were not detected.

Animals↗
PubMedDate not supplied

Comparison of the efficacy and safety of nifedipine coat-core versus amlodipine in the treatment of patients with mild-to-moderate essential hypertension. Hypertension Study Group.

The antihypertensive efficacy and safety of once-daily nifedipine coat-core was compared with that of once-daily amlodipine in a multicenter, prospective, double-blind, randomized, parallel-group study in which titration was based on response. The study consisted of a 2-week, single-blind, placebo run-in period followed by an 8-week double-blind treatment period. Double-blind treatment began with nifedipine coat-core 30 mg or amlodipine 5 mg. After 4 weeks of double-blind therapy, patients with a trough seated diastolic blood pressure (DBP) > or = 90 mm Hg received an increased dose of nifedipine coat-core (60 mg) or amlodipine (10 mg). A total of 207 patients received the study medication at 12 private-practice medical centers. Ambulatory blood pressure monitoring (ABPM) was performed at six medical centers with 38 nifedipine coat-core and 37 amlodipine patients. Data from 176 patients were valid for the primary efficacy analysis. Treatment groups were well matched with respect to baseline demographic and disease characteristics. During the study period, 59 (65.6%) nifedipine coat-core patients remained on their original 30-mg dose of study medication compared with 52 (60.5%) amlodipine patients who remained on the 5-mg starting dose. Mean trough blood pressure at baseline was 160.9/101.9 mm Hg in the nifedipine coat-core patients compared with 160.5/101.8 mm Hg in the amlodipine patients. Mean trough blood pressures at end point were 141.3/85.5 mm Hg and 140.7/85.9 mm Hg in the nifedipine coat-core and amlodipine groups, respectively. Equivalence between the two treatment groups was demonstrated based on the difference between amlodipine and nifedipine coat-core in the change from baseline in trough seated DBP (90% confidence interval, -0.50 to 2.59). Systolic blood pressure and 24-hour ABPM data supported the equivalent antihypertensive efficacy of the two treatments. Both drugs were well tolerated and had similar safety profiles. Nineteen patients in the amlodipine group experienced at least one adverse event compared with 12 in the nifedipine coat-core group. The amlodipine patients tended toward a later occurrence of adverse events plus a greater number of events, particularly edema and gastrointestinal symptoms. More patients in the nifedipine coat-core group (n = 3) than in the amlodipine group (n = 1) discontinued treatment because of adverse events.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMedDate not supplied

A novel platelet-derived renal vasoconstrictor agent in normotensives and essential hypertensives.

Platelet homogenates from 200 ml blood of essential hypertensives (n = 28) and normotensives (n = 13) were deproteinized and separated by gel chromatography. The fractions obtained were then tested for vasopressor activity in the isolated perfused rat kidney. In both normotensives and hypertensives, two vasopressor fractions appeared. There was no difference in vasopressor activity in the first vasoactive fraction between normotensives and hypertensives. In the second vasoactive fraction, the hypertensive patients showed a significant higher activity than the normotensive subjects (increase in perfusion pressure by 35.9 +/- 11.5 vs. 6.8 +/- 5.3 mmHg, p less than 0.01). This vasopressor fraction was not inhibited by saralasin, phentolamine, ketanserin, nitroprusside and daltroban and was effective after pretreatment with indomethacin and reserpine and in enzymatically deendothelialized kidneys. The effect was reduced by nifedipine and unchanged by heating the fraction at 100 degrees C and by incubation with proteinase K. It is concluded that a yet unidentified platelet-derived vasopressor agent may contribute to the enhanced vasoconstriction in essential hypertension.

Adenosine Triphosphate↗
PubMedDate not supplied

Effects of protein kinase C activation on intracellular Ca2+ distribution in vascular smooth muscle cells of spontaneously hypertensive rats.

Protein kinase C is known to influence contraction in vascular smooth muscle cells by Ca(2+)-dependent and Ca(2+)-independent mechanisms. In the present study, the effect of protein kinase C activation by phorbol 12-myristate 13-acetate on resting cytosolic free Ca2+ and on cellular Ca2+ pools was assessed in cultured rat aortic muscle cells using fura 2. Cellular Ca2+ pools were evaluated with the selective inhibitor of the sarcoplasmic Ca2+ ATPase, thapsigargin. In normotensive vascular smooth muscle cells, protein kinase C activation caused a redistribution of Ca2+ from the thapsigargin-sensitive pool into the cytoplasm, whereas, in hypertensive cells, no significant effect of protein kinase C activity on cellular Ca2+ distribution was found. It is concluded that protein kinase C modulates the amount of Ca2+ stored in the thapsigargin-sensitive calcium stores. In hypertensive cells, the regulation of Ca2+ pools by protein kinase C is disturbed.

Animals↗
PubMedDate not supplied

Mechanism of the action of angiotensin-converting enzyme inhibitors on agonist-induced Ca2+ influx.

To evaluate the direct effects of the angiotensin-converting enzyme (ACE) inhibitors, captopril, enalaprilat, enalapril (a prodrug without therapeutically significant ACE inhibitory effect) and ramiprilat, on cellular calcium metabolism, the cytosolic free calcium concentration was measured in cultured rat vascular smooth muscle cells using the fluorescent dye, fura-2. Preincubation with captopril, enalaprilat, enalapril, or ramiprilat for 40 min significantly reduced the angiotensin II-induced transplasma membrane calcium influx but did not influence the angiotension II-induced calcium release from internal stores. Captopril and ramiprilat also inhibited arginine vasopressin, but not the thapsigargin-, norepinephrine-, or the BayK 8644-induced changes in cytosolic calcium. Phorbol 12-myristate 13-acetate pretreatment for 30 s caused an increase in the angiotensin II-induced rise in cytosolic calcium. Although both captopril and verapamil reduced responses to angiotensin II to similar extents, only verapamil blocked the ability of phorbol 12-myristate 13-acetate to enhance responses to angiotensin II. It is concluded that ACE inhibitors modulate the effects of some but not all agonist-induced transplasma membrane calcium influx.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

Diadenosine polyphosphates increase cytosolic calcium and attenuate angiotensin-II-induced changes of calcium in vascular smooth muscle cells.

The effects of diadenosine tetraphosphate (AP4A), diadenosine pentaphosphate (AP5A), and diadenosine hexaphosphate (AP6A) on the cytosolic free calcium concentration ([Ca2+]i) were evaluated in cultured rat vascular smooth muscle cells (VSMC) using the fluorescent dye technique. A concentration-dependent increase of [Ca2+]i by AP4A, AP5A, and AP6A was observed in VSMC. Additions of 10 micromol/l AP4A, AP5A, and AP6A significantly increased [Ca2+]i in VSMC by 224 +/- 98 nmol/l (n = 6; p < 0.01, 205 +/- 27 nmol/l (n = 14; p < 0.01), and 269 +/- 98 nmol/l (n = 5; p < 0.05), respectively. Additions of AP4A, AP5A, and AP6A only 120 s prior to angiotensin II (Ang II) administration significantly attenuated the Ang-II-induced changes of [Ca2+]i in VSMC from 1,053 +/- 174 nmol/l to 283 +/- 42 nmol/l, 591 +/- 112 nmol/l, and 477 +/- 79 nmol/l, respectively (each p<0.01) as compared to the control). The AP6A-induced changes of [Ca2+]i were inhibited by the blockers of P2 purinoceptors, suramin and pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid, but not by the inhibitor of P2y purinoceptors, reactive blue. Adenosine triphosphate (ATP) also increased [Ca2+]i in VSMC, whereas the purinoceptor P2x agonist, alpha,beta-methylene-ATP, had no effect on [Ca2+]i in VSMC. Therefore diadenosine polyphosphates may induce changes of [Ca2+]i by interacting with purinoceptors and may be involved in local regulation of vascular resistance evoked by the Ca(2+)-dependent contractile response of VSMC.

Adenosine Triphosphate↗
PubMedDate not supplied

Ambulatory 24-h blood pressure monitoring in essential hypertensives treated with the angiotensin-converting enzyme inhibitor ramipril.

A double-blind, crossover study was carried out on the antihypertensive effect of 5 mg ramipril. Continuous 24-h blood pressure monitoring was performed on 15 essential hypertensives [mean (+/- SD) blood pressure 155.2 +/- 6.5/101.3 +/- 4.8 mmHg], 24 h prior to treatment and 48 h after having received either antihypertensive therapy or placebo; the patients taking part in the study had not taken any antihypertensive treatment 4 weeks prior to the beginning of the trial. After receiving 5 mg ramipril the mean 24-h blood pressure was significantly (P less than 0.05) reduced to 148.3 +/- 5.8/91.5 +/- 5.5 mmHg. After 48 h the blood pressure increased to 153.1 +/- 4.8/96.0 +/- 6.4 mmHg. In the placebo group there was only a slight, non-significant reduction in blood pressure on day 1 (154.3 +/- 6.9/97.3 +/- 5.7 mmHg) and during day 2 the blood pressure increased to 155.4 +/- 5.3/99.5 +/- 5.9 mmHg. The results showed that a once-daily administration of 5 mg ramipril produced a reduction in blood pressure, which lasted 24 h. This simple therapeutic regime offers the advantage of being easy for patients to follow and, therefore, promotes compliance with therapy.

Adult↗