PubMed Health⌕ Search

Biomedical subjects

J C Prieto

Publications and source records attributed to J C Prieto.

159 records · Page 9Linked to original sources
PubMed1978

Effect of prolonged fasting upon insulin and glucagon secretion from isolated rat pancreatic islets.

To study insulin-glucagon interrelationships in the regulation of pancreatic islet functions, glucose-mediated insulin and glucagon secretion have been studied in isolated pancreatic islets from fed and from 4 and 8-day fasted rats. At low glucose levels (50 mg %) a continuous decrease of insulin and increase of glucagon secretion were observed during prolonged fasting. High glucose concentrations 300 mg %) stimulated insulin and inhibited glucagon secretion until 4 days, but did not cause any effect after 8 days fasting. These results suggest that the secretory mechanisms of the two hormones may have a common basis.

Animals↗
PubMed1978

Binding activity regulation of rabbit skeletal muscle adenosine 3'-5'-monophosphate-dependent protein kinases.

A cAMP-dependent protein kinase has been isolated from rabbit muscle and purified. The affinity constant of the enzyme for the nucleotide is Ka = 9.3 X 10(-9) M, with a Vmax = 0.013 X 10(12) moles bound cAMP/1 microgram protein. The influence exerted by different factors is studied: a) Inhibitor (I) of kinase activity: increases the binding capacity for cAMP, by percentages which depend on the amount of I. In the presence of inhibitor (120 microgram/100 microliter) the affinity constant is Ka = 4.1 X 10(-9) M, without change in Vmax. b) Effect of pH: it has a complex influence over binding, being also regulated by cAMP concentration. The positive effect on binding of ionic and bovine serum albumin concentrations, and the negative effect of enzyme preincubation before additions of (H3) cAMP, have also been studied. The importance of these effectors to obtain a high degree of sensitivity in the binding protein method has been assertained.

Animals↗
PubMed1976

hCS regulation during pregnancy.

In order to define the homeostatic mechanisms which affect the secretion of human chorionic somatomammotropin (hCS), we have determinated its plasma levels by a radioimmunoassay method in normal, prediabetic, and chemically diabetic pregnant women in basal conditions and after stimuli. Oral glucose failed to modify hCS plasma levels as also did continuous intravenous glucose infusion. Rapid acute intravenous glucose decreased them, suggesting that only sudden changes in maternal plasma glucose can exert a regulatory effect on hCS secretion. In travenous arginine increased hCS levels, new evidence of the great similarity of structure and function between growth hormone and hCS.

Administration, Oral↗
PubMedDate not supplied

Activation of cyclic AMP-dependent protein kinase by VIP in blood mononuclear cells.

Vasoactive intestinal peptide stimulated cyclic AMP-dependent protein kinase activity in human blood mononuclear cells. The simultaneous presence of a phosphodiesterase inhibitor was required to elicit maximal activation. The apparent Ka value of half the maximal stimulation was about 60 pmol. Secretin exhibited a 170-times lower potency. Other peptides such as glucagon or insulin had no effect even at 1 microM.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

Interaction of somatostatin with isolated cytosol from rabbit renal papilla.

Specific binding sites for somatostatin have been characterized in cytosolic fraction of rabbit renal papilla. The interaction of 125I-Tyr11-somatostatin with cytosolic fraction was rapid, reversible, specific, saturable and dependent on temperature. At 25 degrees C the binding data were compatible with the existence of two classes of binding sites: a high-affinity class with a Kd = 57.7 nM and a low-affinity class with a Kd = 217.4 nM. Somatostatin binding sites exhibited a high degree of specificity since neuropeptides such as Leu-enkephalin, neurotensin, substance P, vasopressin and vasoactive intestinal peptide behaved as ligands with null or very low affinity.

Animals↗
PubMedDate not supplied

Somatostatin binding to dissociated cells from rat cerebral cortex.

A method has been developed for the study of somatostatin (SS) binding to dissociated cells from rat cerebral cortex. Binding of [125I] [Tyr11]SS to cells obtained by mechanical dissociation of rat cerebral cortex was dependent on time and temperature, saturable, reversible and highly specific. Under conditions of equilibrium, i.e., 60 min at 25 degrees C, native SS inhibited tracer binding in a dose-dependent manner. The Scatchard analysis of binding data was linear and yielded a dissociation constant of 0.60 +/- 0.08 nM with a maximal binding capacity of 160 +/- 16 fmol/mg protein. The binding of [125I] [Tyr11]SS was specific as shown in experiments on tracer displacement by the native peptides, SS analogues, and unrelated peptides.

Animals↗
PubMedDate not supplied

Adenylyl cyclase stimulation by VIP in rat seminal vesicle membranes.

Vasoactive intestinal peptide (VIP) stimulated adenylyl cyclase activity in membranes from rat seminal vesicle. GTP potentiated the stimulatory effect of VIP so that it was routinely included at 10 microM. The stimulation of adenylyl cyclase by VIP was time and temperature dependent. The response was linear with time up to 15 min at 30 degrees C. Half-maximal adenylyl cyclase activation (in the presence of 10 microM GTP) was achieved at 3.0 nM VIP. The enzyme activity increased about 150% with respect to basal values at the maximal VIP concentration tested (1 microM). The relative potency of peptides upon stimulation of adenylyl cyclase activity was: VIP greater than helodermin greater than peptide histidine isoleucinamide greater than rat growth hormone-releasing factor. Other agents like GTP (0.1 mM), GppNHp (0.1 mM), forskolin (0.1 mM) and sodium fluoride (10 mM) increased the adenylyl cyclase activity 1.8-, 4.4-, 6.7- and 2.4-fold, respectively. Taken together, the presence of VIP in nerve terminals innervating the seminal vesicle of rats and the existence of VIP receptors coupled to adenylyl cyclase strongly suggest a physiological role for this neuropeptide in the modulation of seminal vesicle cell function.

Adenylyl Cyclases↗
PubMedDate not supplied

Differential effect of arachidonic acid on the vasoactive intestinal peptide receptor/effector system in rat prostatic epithelium during sexual maturation.

The effects of alterations in the membrane lipid environment on vasoactive intestinal peptide (VIP) binding and VIP-stimulated cyclic AMP accumulation have been analyzed by arachidonic acid treatment of prostatic epithelial cells from rats at puberty and maturity, two critical developmental periods with characteristic lipidic and androgenic statuses. Treating cells with 0.1 mM arachidonic acid for 15 min at 37 degrees C increased the affinity of VIP receptors and the potency of the neuropeptide (up to five times) in the formation of cyclic AMP at maturity, but not at puberty. The average plasma membrane fluidity (as measured by fluorescence polarization of diphenylhexatriene) remained unmodified after arachidonic acid treatment of cells. The modifications observed in mature rats were specific for the VIP receptor/effector system, since cyclic AMP stimulation by isoproterenol or forskolin was not affected by cell treatment with arachidonic acid. These results are compatible with the existence of a particular lipidic microdomain surrounding the VIP receptor in the cell membrane that would be altered by exposure to arachidonic acid (either directly or through conversion of arachidonic acid to its metabolites, as suggested by experiments on inhibition of the arachidonic acid cascade). This would make it possible for the activation of protein kinase C to phosphorylate VIP receptors in cells from mature rats, but not in those from pubertal animals with a very different membrane lipid composition (as suggested by the corresponding values of membrane fluidity and transition temperature).

Aging↗
PubMedDate not supplied

Modification of somatostatin content and binding in jejunum from celiac children.

The concentration of somatostatin was studied in controls as well as in plasma and jejunal mucosa from celiac children with and without jejunal villous atrophy. The binding of somatostatin to cytosolic fraction, isolated from jejunal mucosa from celiac patients and controls, was also investigated. Fasting plasma somatostatin concentrations were not significantly different among the various groups studied. However, the jejunal somatostatin content was significantly higher in the group of celiac children with subtotal villous atrophy as compared to control group and celiac children with normal villous architecture. The binding of somatostatin to cytosol of jejunal mucosa was significantly decreased in the group of celiac children with subtotal villous atrophy. The present results suggest that somatostatin may be involved in the pathophysiological processes of celiac disease.

Binding Sites↗
PubMedDate not supplied

[Vagal influence in experimental arrhythmias caused by dopamine].

Dopamine induced cardiac arrhythmias in control and reserpine-treated rats which was successfully++ prevented by functional inhibition of the parasympathetic system. Both EKG and intracarotid mean blood pressure were recorded through a polygraph. Animals were anesthetized with urethane, intravenously heparinized and enhanced its spontaneous pulmonary ventilation with a tracheal cannula. Dopamine (50, 100, 200 and 400 micrograms/100 g,) produced cardiac arrhythmias characterized by atrioventricular block, ventricular premature depolarization and ventricular tachycardia. The parasympathetic inhibition resulting from bilateral vagotomy or atropine injection (1 mg/kg i.v.) induced a significant reduction in the arrhythmia frequency. A vagal reflex originating in great vessel baroreceptors is postulated as the ensuing mechanism. Vagal inhibition seems to be efficacious to prevent cardiac arrhythmias and lowering mortality rate.

Animals↗
PubMedDate not supplied

[Hypotensive effect of dopaminergic agonists in the rat].

Dopamine, Bromocriptine and Apomorphine produce arterial hypotension in the rat, but so far remains to be established if the phenomenon takes place at the presynaptic or postsynaptic nerve terminal. Present study deal with the locus of action of these substances. Rats were anesthetized with urethane i.p. and heparinized, maintaining the spontaneous pulmonary ventilation through a tracheal cannula. EKG and intracarotid mean blood pressure were recorded through a polygraph. Dopamine as well as Bromocriptine (3.12 to 25 mu/100 g both) and Apomorphine (0.125 to 4.0 micrograms/100 g) caused a dose-related hypotension, together with moderate bradycardia and in Apomorphine treated rats, atrioventricular block. In 28 animals, chemical sympathectomy was performed with 6-OH-DA (3 mg/100 g i.p.) and 2 hours later the three substances were injected. Under these conditions, Dopamine raised the blood pressure (p less than 0.001) while Apomorphine lessened the hypotensive effect (p less than 0.02) and Bromocriptine caused no changes on this regard. It is suggested that the main effect of Dopamine on blood pressure lies at a prejunctional nerve terminal level whereas Bromocriptine acts at the effector organ post junctional level. In Apomorphine effect it might be mainly involved a prejunctional component.

Animals↗