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Biomedical subjects

G Velasco

Publications and source records attributed to G Velasco.

64 records · Page 4Linked to original sources
PubMed1985

Adenylate cyclase from rabbit small intestine: activation by cholera toxin and interaction with calcium.

The stimulation of adenylate cyclase in various fractions of plasma membranes from rabbit small intestinal epithelium has been studied. In crude plasma membranes cholera toxin activated 5-fold at 10 micrograms/ml; vasoactive intestinal peptide (VIP) activated at concentration from 10(-8) to 10(-7) M, the maximal stimulation being 6-fold. Fluoride activated 10-fold at 10 mM. VIP-stimulated enzyme was inhibited by Ca2+ concentrations in the micromolar range. In the presence of calmodulin a biphasic response was obtained. At low Ca2+ concentration (4 x 10(-9)-6 x 10(-8) M) the enzyme was activated. As the Ca2+ concentration was increased the enzyme was concomitantly inhibited. We have investigated the mechanism by which cholera toxin activates intestinal adenylate cyclase. We have found that cholera toxin catalyzed incorporation of 32P into proteins located in the brush-border membrane whose molecular weights are in the range of 40-45kDa. These membranes bind [3H]GTP with a Kd of 1.8 x 10(-7) M. In contrast, basal lateral membranes do not contain any protein which becomes labeled in a toxin-dependent manner when incubated with cholera toxin and [32P]NAD. The modification of brush-border membrane protein occurred in spite of the absence of adenylate cyclase in these membranes. Adenylate cyclase in basal lateral membranes was poorly activated by cholera toxin as compared to crude plasma membranes. On the other hand, the ability of VIP and fluoride to activate the enzyme was enhanced in basal lateral membranes with respect to crude membranes. The results are discussed in relation to the mechanism by which cholera toxin activates adenylate cyclase in intact intestinal cells.

Adenosine Diphosphate Ribose↗
PubMed1984

Regulation by calcium and calmodulin of adenylate cyclase from rabbit intestinal epithelium.

The effect of calcium on adenylate cyclase from rabbit small intestine has been studied using a particulate preparation obtained from isolated epithelial cells. Both basal and vasoactive intestinal peptide-stimulated activities were inhibited by calcium concentrations in the micromolar range. In the presence of calmodulin, a biphasic response was obtained. At low calcium concentration (4 X 10(-9)-6 X 10(-8) M) the enzyme was activated up to 50%. As the Ca2+ concentration was increased, the enzyme was concomitantly inhibited. Half-maximal inhibition of calmodulin-dependent activity was obtained at 1 microM free Ca2+. The activation of the enzyme was also dependent on the concentration of Mg2+. At less than 1 microM Ca2+, the enzyme exhibited a biphasic response, being activated at below 3 mM Mg2+ and inhibited at higher concentrations. At Ca2+ concentrations that were inhibitory, the enzyme did not show the biphasic response to Mg2+. At concentrations above 3 mM, the maximal rate (Vmax) remained constant. Vmax was inversely proportional to the concentration of Ca2+ present. Calmodulin altered Vmax when acting on vasoactive intestinal peptide-stimulated enzyme. Calmodulin had no effect on the Km for hormone activation. The calmodulin-dependent activity was inhibited by incubation with trifluoperazine.

Adenylyl Cyclases↗
PubMed1984

RNA electropherotypes of human rotaviruses from North and South America.

Between April 1979 and December 1982, viral agents were found in 231 of 695 children admitted to the Texas Children's Hospital with gastroenteritis. Electron microscopic analysis showed that rotaviruses were the most common viral agents, and a seasonal pattern of rotavirus disease was observed. The migration patterns of the RNA segments of these rotaviruses on electrophoresis in polyacrylamide gels were compared with those of rotaviruses collected from other areas of the United States of America and from Argentina, Colombia and Mexico. A number of different RNA electropherotypes were found, including some patterns not previously reported.

Child↗
PubMedDate not supplied

Effect of chronic electrical stimulation of the centromedian thalamic nuclei on various intractable seizure patterns: II. Psychological performance and background EEG activity.

We studied the effect of electrical stimulation of centromedian thalamic nuclei (ESCM) on seizure control and paroxysmal EEG activity in 23 patients. We report the effect of chronic ESCM on psychological performance and background EEG activity of patients with various intractable seizure patterns. In each patient, a simple specifically designed neuropsychological scales (one for adults and one for children) was administered at the end of the baseline (BL), ESCM, and poststimulation (Post) periods; and 14 consecutive EEG recordings during these periods were performed to determine the degree of neuropsychological improvement and the temporal course of EEG changes. A significant increase in psychological scores and the number of background EEG waves per 10 s was noted in groups A (generalized tonic-clonic seizures, GTC), C (complex partial seizures, CPS), and D (generalized tonic seizures) and the total group of patients from BL to ESCM and from BL to Post periods. Group B patients showed a substantial increase (partial motor seizures) during the same periods. Improvement on psychological performance correlated better with age and baseline degree of deterioration than with the nature of the particular psychological improvement in any given subtest. The improvement in EEG background rhythm was most noticeable at the end of ESCM and at the beginning of the Post periods. Complete normalization of neuropsychologic scores and EEG rhythms was rare, but improvement was significant for both. Psychological scores increased from BL 14 +/- 2 to ESCM 21 +/- 2 and Post 23 +/- 2 (normal expected 26), and EEG background rhythm increased from BL 42 +/- 2 to ESCM 62 +/- 2 and Post 54 +/- 2 EEG waves/10 s. (normal expected > 80).

Adolescent↗
PubMedDate not supplied

[L-arginine-nitric oxide pathway in hemodialysis].

Nitric oxide (NO) is derived from the metabolism of the amino acid L-arginine by NO synthase (NOS). One of the forms of NOS (i-NOS) can be induced by cytokines, bradykinin and endotoxin. During hemodialysis (HD), blood-dialysis membrane interaction can induce production of these mediators. HD can also induce changes of asymmetrical dimethylarginine (ADA), a potent inhibitor of NOS. The aim of this study was to investigate the effect of HD, using cuprophane (C, polyacrilonytrile (PAN) and special polyacrylonitrile (SPAN) membranes, on cellular NOS activity, and changes of plasma tumor necrosis factor (TNF-alpha), bradykinin, ADA and nitrate concentration. Before HD, cellular i-NOS activity was similar with the three membranes. Cuprophane HD induced a significant increase in i-NOS activity from 31 +/- 10 to 48 +/- 12 fmol-1 10(6) cells (p < 0.05). No changes were found in PAN and SPAN HD. The TNF-alpha values increased significantly during HD with C (56 +/- 6 vs 47 +/- 5 pg/ml, p < 0.05). No changes of bradykinin concentration were found during HD. A significant decrease of ADA and nitrate levels was observed during HD with three membranes. No significant correlation was found between percentage increase in i-NOS activity and the changes in other parameters. These findings suggest that HD with bioincompatible membranes can induce activation of cellular i-NOS.

Adult↗
PubMedDate not supplied

[Hormonal profile and participation of nitric oxide in salt-sensitive and salt-resistant essential arterial hypertension].

Recent studies have shown that cardiovascular events and end-organ damage occur more frequently in patients with salt-sensitive essential hypertension (SH) than in salt-resistant essential hypertension (RH). Nitric oxide (NO) plays an important role in regulating the pressure-natriuresis relationship. Therefore impaired NO synthesis may produce or aggravate salt-sensitive hypertension. This study was conducted to determine the hormonal levels and nitric oxide metabolites in hypertensive patients. 25 patients underwent salt sensitivity testing. 24 h ambulatory blood pressure was recorded after a 5-day period on low salt diet (20 mEq/d) and after a 5-day period on a high salt diet (200 mEq/d). Subjects showing > or = 10 mmHg increase in mean BP when changing from low to high dietary salt intake were classified as salt sensitive and as salt resistant when the BP changes were < 10 mmHg. Based on BP recordings 13 patients were characterised as white coat hypertension (WC), 13 patients as salt resistant (SR) and 12 as salt sensitive (SS). A significative relationship was seen between plasma glucose-insulin concentration and body mass index. The ventricular mass index was similar in SS and SR patients. The plasma uric acid, triglicerides and PAI-I were elevated in SS compared with SR, and control group (C). During low sodium intake, plasma renin and aldosterone were decreased in SS compared with SR, and C. No differences in plasma catecholamines or their changes with intake sodium modifications were seen among the patients. During high sodium intake urinary NO excretion increased in SR (38 +/- 9 vs 18 +/- 2 mg/g creat), and C (24 +/- 2 vs 16 +/- 3 mg/g creat) (p < 0.01) but not in SS patients (21 +/- 3 vs 26 +/- 4 mg/g creat). The NO excretion changes showed negative correlation with BP changes (r = 0.49, p < 0.01). During low sodium intake, SR and SS patients showed a normal nocturnal decrease of BP (dippers). During high sodium intake SS patients became non-dippers. Our results showed that patients with salt sensitive hypertension displayed a suppressed renin-aldosterone system, an attenuated nocturnal decline in blood pressure on high-salt diet and an impairment of endothelial function. The relationship between urinary nitrate excretion and arterial pressure suggest that the salt sensitivity of arterial pressure may be related bo blunted generation of endogenous nitric oxide.

Adult↗
PubMedDate not supplied

Quinapril versus enalapril in the treatment of mild-to-moderate essential hypertension.

Two angiotensin converting enzyme inhibitors, quinapril and enalapril, were evaluated for comfort, safety, and efficacy in the treatment of mild-to-moderate hypertension. After a four-week placebo period, 53 hypertensive outpatients (diastolic blood pressure, 95 to 115 mmHg), aged 31 to 66 years, were randomly assigned to received 10 to 20 mg of quinapril or enalapril daily for 12 weeks. Two hours after the first dose of each drug, sitting and standing systolic and diastolic blood pressures were reduced significantly from baseline values; these reductions were maintained for the 12 weeks of treatment, with no significant between-group differences. No changes in heart rate were noted. Treatment was discontinued in three quinapril-treated patients and in one enalapril-treated patient because of treatment side effects. It is concluded that both quinapril and enalapril are safe and effective in the treatment of mild-to-moderate hypertension.

Adult↗
PubMedDate not supplied

Mechanism of nafazatrom-induced inhibition of rat uterus contractions in vitro.

Nafazatrom inhibits, in a dose-dependent way, the amplitude and frequency of the rhythmic contractions induced by oxytocin (4 mU/ml), as well as the methacholine (10(-5) M)- and CaCl2 (10 mM)-induced contractions, and the phasic response to KCl (60 mM); similarly, it inhibits the tonic contraction induced by KCl (60 mM) and oxytocin (10 mU/ml). A single concentration of nafazatrom (10(-4) M) also inhibits the uterine contractions caused by carbachol (10(-4) M) and prostaglandin F2 alpha (10(-6) M). CaCl2 (0.1-10 mM) only partially reverses the inhibition produced by nafazatrom on the KCl-induced tonic contractions. Bay K 8644 (3 x 10(-10)-3 x 10(-7) M) reverses the inhibition by 10(-4) M but not by 3 x 10(-4) M of nafazatrom on the CaCl2-induced contractions. Nafazatrom also inhibits, in a dose-dependent way, the calmodulin-dependent phosphodiesterase activity. Our results would suggest that, independently of its 5-lipoxygenase blocking activity, nafazatrom inhibits the contractions of the rat uterus by inhibiting the calmodulin activity and, presumably, by reducing the influx of extracellular calcium and/or the mobilization of intracellular calcium.

3',5'-Cyclic-AMP Phosphodiesterases↗