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At least 973 records · Page 54Linked to original sources
PubMed1990

[The clinical profile of hypertensive patients can predict the need for combining a second or third drug with atenolol in the initial treatment of light and moderate essential arterial hypertension].

In this study the clinical, biological, radiologic, electrocardiographic, and hormonal characteristics of 80 patients with slight or moderate essential arterial hypertension in whom the treatment with atenolol alone or associated with chlorthalidone or with a third agent normalized the arterial pressure during a period of one year, are revised. Atenolol given alone at the dose of 50 to 100 mg per day normalized the blood tension in 44 (55%) patients, in 26 cases (32.5%) the association of chlorthalidone 25 mg/day was required, and in the remaining 10 patients (12.5%) a third pharmacologic agent was needed. Patients who required the association of three agents (group C) had systolic arterial pressures significantly higher than those observed in patients treated with atenolol alone (group A) (176.6 +/- 14.3 vs 161.4 +/- 12.9 mmHg, p less than 0.01) and higher to those measured in patients who required the association of chlorthalidone (group B) (176.6 +/- 14.3 vs 162.8 +/- 15 mmHg, p less than 0.05). On the other hand the 44 hypertensive patients controlled with monotherapy showed a lower incidence of cardiovascular complications (6.8% in group A, 38.5% in group B, and 30% in group C, p = 0.0042), they required acute treatment for hypertensive crisis (34.1% in group A, 73.1% in group B, and 66.7% in group C, p = 0.0041), and they showed electrocardiographic signs of left ventricular hypertrophy or overload (26.2% in group A, 60% in group B, and 42.9% in group C, p = 0.0228).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

[Eccrine poroma: its histogenesis and review of the literature].

It has been done an analysis of a case of eccrine porome, based on the morphology, considering the actual tecnical publications on the matter. The morphogenesis of the formation of this nevoid tumor is established by the continuity between the main body of the tumor and the underneath eccrine sweat glands. These glands present signs of hyperplasia, which in the highest levels present destructuration of the excretory duct and morphological modifications of the cells which are conditioned by the functional adaptation at different levels. In this way there is proliferation of structures, similar to the different parts of syringuium and acrosyringuium producing this hamartomatous neoformation.

Adenoma, Sweat Gland↗
PubMed1989

Abnormal erythrocyte sodium leak in a subset of essential hypertensive patients.

We measured the ouabain- and bumetanide-resistant Na+ efflux in Mg2+-sucrose medium (passive Na+ leak) in erythrocytes from 30 normotensive controls and 72 essential hypertensive patients. The mean values (+/- SEM) of the rate constant of Na+ leak (kpNa) were not significantly different between normotensives and hypertensives. Nevertheless, using the 95% confidence limits of the kpNa (in 10(-3).h-1) in the normotensive group as a cut-off point, 7 (9.7%) essential hypertensives exhibited increased values (58.96 +/- 10.12) when compared with the other 65 patients (23.86 +/- 0.74). revealing increased passive Na+ permeability in the former (leak "+" hypertensives). Na+ fluxes depending on the Na+-K+ pump, outward Na+-K+ cotransport, and Na+-Li+ countertransport were also measured in fresh erythrocytes from the same 72 patients. Three of them (4.2%) exhibited decreased values of ouabain-sensitive Na+ efflux and 6 (8.3%) of bumetanide-sensitive Na+ efflux, while 8 patients (11.1%) showed increased values of Li+-stimulated Na+ efflux and, finally, 48 patients (59.7%) did not present any evident abnormality in these Na+ transport systems. No differences were observed between leak "+" hypertensives and the remaining 65 patients when both basal erythrocyte Na+ content and clinical parameters of hypertension were compared. However, Na+ efflux depending on the outward Na+-K+ cotransport was significantly higher in the leak "+" hypertensive subset (299.43 +/- 43.18 vs 181.52 +/- 10.76 mumol.(l cells.h)-1; P = 0.0078), suggesting a compensatory phenomenon. Enhancement of Na+ permeability detected in 3% to 16% of essential hypertensives may be implicated in the pathogenesis of primary hypertension.

Adult↗
PubMed1989

Electrical membrane properties of a cell clone derived from human nonpigmented ciliary epithelium.

Intracellular potentials were measured in a SV-40 virus-transformed cell clone derived from human nonpigmented ciliary epithelium using the microelectrode technique. (1) Membrane potential averaged -50.2 mV (+/- 0.6, n = 207). (2) Increasing the extracellular K+ concentration depolarized the membrane voltage. The amplitude of this potential response was reduced in the presence of 1 mM Ba2+. (3) Superfusing the cells with a Ca2+-free solution containing 1 mM EGTA depolarized the intracellular potential and diminished the voltage response upon increasing extracellular K+. (4) Extracellular alkalinization hyperpolarized the membrane potential and increased the voltage amplitude on increasing extracellular K+. (5) Addition of ouabain immediately reduced the intracellular potential. Removing extracellular K+ depolarized membrane voltage, readdition of K+ after K+ depletion transiently hyperpolarized intracellular voltage. Both potential responses were inhibited in the presence of ouabain. (6) Replacing extracellular Cl- by cyclamate resulted in a transient depolarization followed by a hyperpolarization. In the presence of SITS or DIDS (greater than or equal to 0.1 mM) the electrical responses of the cell membrane to Cl- replacement were blocked. We conclude that cultured human nonpigmented ciliary epithelial cells possess an electrogenic Na+/K+-ATPase, a K+ conductance modulated by Ca2+ and pH, and a Cl- conductance sensitive to stilbene derivatives.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Ultrastructure and light microscopical study of a Leydig cell tumor of the testis associated with bilateral gynaecomastia.

Light and electronmicroscopic study of a Leydig cell testicular tumor in an 18-year-old male is presented. Bilateral gynaecomastia and normal hormonal blood levels were found. Emphasis on the diagnostic value of electronmicroscopy is remarked upon, based on the following ultrastructural characteristics of the cells; 1) Ovoid shaped nuclei with ondulating contours and dispersed and homogeneous chromatin, 2) Rich agranular endoplasmic reticulum with frequent special modifications, such as membranous whorls with a central cytoplasmic mass or lipid droplets, 3) Numerous mitochondria with occasional tubular cristae, 4) Numerous lipid vacuoles. Other structures also identified in this tumor are Reinke crystalloids, cytoplasmic microbodies, myelin figures, gap-type junctional complexes and paracrystalline inclusions of Payer type E, which are less common.

Adolescent↗
PubMed1989

Receptor-mediated phosphoinositide hydrolysis in human ocular ciliary epithelial cells.

The hydrolysis of phosphoinositides (PI) in peripheral tissues can be stimulated by a number of putative neurotransmitters and this stimulation can be blocked by specific antagonists. Epithelial cells derived from the nonpigmented layer of the ocular ciliary epithelium were transfected by simian virus 40 and grown in culture to semiconfluency. The cells were incubated in 3 microCi/ml of (3H)-myoinositol for 2 days. The accumulation of inositol phosphates in response to several agonists (carbachol, 1 mM; ATP, 100 microM; arginine vasopressin, 1 microM; and phenylephrine, 100 microM) was determined for times ranging from 5 sec to 15 min. In the presence of 10 mM LiCl, the maximum net production of the (3H)-inositol phosphates (expressed as a percent of conversion of (3H)-phospholipids) was approximately 7.5% for inositol-1 phosphate, 0.5% for inositol-1,4 bisphosphate, and 1% for inositol-1,4,5 trisphosphate. Carbachol elicited PI hydrolysis with an EC50 value of 39 +/- 9 microM. The EC50 values obtained for arginine vasopressin and ATP-initiated PI breakdown were 32 +/- 10 nM and 11.9 +/- 1 microM, respectively. Phenylephrine alone failed to stimulate the production of (3H)-inositol phosphates in these cells. The production of all (3H)-inositol phosphates in response to carbachol (1 mM) was inhibited by atropine (Ki = 0.3 nM) and the selective muscarinic antagonists 4-DAMP (Ki = 4.2 nM), pirenzepine (Ki = 102 nM) and AFDX-116 (Ki = 1.49 microM). Thus the muscarinic receptors that are coupled to PI hydrolysis in these cells have the pharmacologic characteristics of the M3 subtype.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1989

Effect of acetylcholine on membrane potential of cultured human nonpigmented ciliary epithelial cells.

Human nonpigmented ciliary epithelial cells (NPE) were grown in tissue culture after transformation with an origin-defective mutant of SV-40 DNA. In these cells membrane potentials (V) were measured using the microelectrode technique. Addition of 10(-4) M acetylcholine led to a bisphasic voltage response. An immediate, transient hyperpolarization was followed by a sustained depolarization below the steady state level. These responses were irreversibly blocked by 10(-5) M atropine. In Ca2+-free media the initial addition of acetylcholine resulted in an unchanged voltage response. A second application of acetylcholine in Ca2+-free solution evoked only an abortive response of V, and further addition had no effect on V. In the presence of Ca2+ channel blockers (10(-5) M verapamil, 1 mM Co2+) the acetylcholine-induced response of the membrane potential was not changed. The initial hyperpolarization induced by acetylcholine was reduced by 33 +/- 3% (n = 6) in the presence of 2 mM Ba2+ and by 79 +/- 6% (n = 6) in the presence of 1 mM quinidine. Moreover, the amplitude of the hyperpolarization was dependent on the extracellular K+ concentration. With increasing extracellular K+ concentration (and decreasing transmembrane K+ gradient) the acetylcholine-induced hyperpolarization was reduced. To further elucidate the role of Ca2+ in the acetylcholine-induced responses, we measured cytoplasmic Ca2+ activity using the fluorescence of intracellularly trapped Fura-2. Cytoplasmic Ca2+ activity increased immediately and transiently upon addition of acetylcholine. We conclude that acetylcholine transiently hyperpolarizes V in cultured human NPE by activation of K+ channels mediated by mobilization of Ca2+ from intracellular stores.

Acetylcholine↗
PubMed1989

Outward Na+-K+-Cl- cotransport function in erythrocytes from essential hypertensives.

We have performed a kinetic analysis of the interaction of the outward Na+-K+-Cl- cotransport system with intra-cellular Na+ in erythrocytes from 30 normotensive controls and 72 patients with essential hypertension. Neither maximal rate of ouabain-resistant, bumetanide-sensitive sodium efflux (Vmax) nor intracellular Na+ content required for half-maximal stimulation (K50%) were significantly different between normotensives and hypertensives. Nevertheless, using 95% confidence limits of the K50% in the normotensive group as a cut-off point, 21 (29.17%) essential hypertensive patients exhibited values above the upper normal limit of 20.11 mmol/l cells, revealing a decreased apparent affinity of outward Na+-K+-Cl- cotransport for internal Na+ ('Co-' hypertensives). The Vmax of Na+-K+-Cl- cotransport exhibited a great variability among hypertensives but 'Co-' patients tended to have increased values of this parameter when compared with the remaining essential hypertensives (959 +/- 84 vs 652 +/- 39 mumol/l cells/h, P = 0.0024). Mean BP values were significantly lower in the 'Co-' subset (121.4 +/- 1.6 mmHg), compared with the remaining 51 hypertensive patients (126.4 +/- 1.3 mmHg, P = 0.0297). We conclude that an abnormal function of outward Na+-K+-Cl- cotransport is present in 19% to 40% of Spanish patients with essential hypertension and this abnormality may be implicated in the mechanisms of hypertension.

Adult↗
PubMed1989

Prone decubitus: a solution to inferior wall attenuation in thallium-201 myocardial tomography.

We propose an efficient method to suppress inferior wall attenuation in 201TI 180 degrees myocardial tomography. We systematically performed redistribution studies in both supine and prone decubitus, assuming that the latter should result in shifting with respect to each other's cardiac structures and diaphragm as well as subphrenic organs possibly responsible for attenuation. The comparison of both studies in 25 normal subjects by visual interpretation and circumferential profiles analysis showed a complete suppression of significant attenuation in the inferior wall in prone studies. In addition and consequently, the standard deviation of activity in this area was markedly reduced and became close to its value in anterior and lateral walls. This simple technique now routinely performed in over 400 patients drastically improves specificity in the evaluation of inferior wall abnormalities by suppressing attenuation artifacts and, incidently, the effect of high individual variability in left phrenic and subphrenic anatomic configuration.

Coronary Disease↗