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Biomedical subjects

R Serio

Publications and source records attributed to R Serio.

63 records · Page 4Linked to original sources

[Esophageal EMG activity in the pigeon (Columbia livia) in vivo].

The pigeon esophageal smooth muscle shows "spontaneous" rhythmic bursts of spikes with increasing discharge frequency from pharynx to crop. There are no slow waves. The changes of the electric pattern induced by pharmacological administrations of atropine, prostigmine, hexamethonium and by asphyxia suggest that the electric activity is myogenic in origin. The innervation plays a role in the control of this activity and it is essential for the functional polarization.

Animals↗

Alpha-adrenergic inhibition of cyclic AMP accumulation in hamster adipocytes. Similarity of receptor with alpha-2 adrenergic receptors.

The present communication shows the effects of several alpha-adrenergic agonists and antagonists on cyclic AMP levels in hamster epididymal adipocytes. In response to ACTH (30 mU/ml) in combination with 1-methyl-3-isobutylxanthine (0.10 mM) or adenosine deaminase (1.0 micrograms/ml), cyclic AMP levels increased to a maximum by 10 min and this level was maintained for another 20 min. Elevated cyclic AMP levels were partially suppressed by the alpha-adrenergic agents clonidine, methoxamine, methyl norepinephrine and phenylephrine. The lowest effective concentration of each of these agonists required to suppress cyclic AMP levels was 10 nM clonidine; 3 microM methoxamine; 10 microM methyl norepinephrine; 10 microM phenylephrine. Clonidine and methoxamine suppressed cyclic AMP levels by nearly 65% while phenylephrine and methyl norepinephrine caused only a 30% decline. Studies of the relative potencies of alpha-adrenergic blocking drugs on prevention of the inhibitor effect of clonidine on cyclic AMP levels disclosed that phentolamine and yohimbine were more potent blockers of clonidine action than phenoxybenzamine and prazosin. The rank order of potencies of agonists at causing suppression of cyclic AMP levels and the rank order of potencies of antagonists of clonidine action suggest similarity of the alpha-adrenergic receptors present on hamster adipocytes, which affect cyclic AMP accumulation to alpha-2 adrenergic receptors.

1-Methyl-3-isobutylxanthine↗

Inhibition of lipolysis in hamster adipocytes with selective alpha-adrenergic stimuli. Functional characterization of the alpha-receptor.

This communication shows the relative potencies of the alpha-agonists clonidine, methoxamine, methyl norepinephrine and phenylephrine in producing inhibition of lipolysis. At cell densities greater than 15 mg cell/ml lipolysis activated by either 1-methyl-3-isobutyl xanthine or adenosine deaminase was inhibited by alpha-adrenergic stimuli with a rank order of potency of clonidine greater than methoxamine greater than methyl norepinephrine; phenylephrine produced a further stimulation of lipolysis. At the same cell density isoproterenol-accelerated lipolysis was inhibited by alpha-adrenergic stimuli with a rank order of potency of phenylephrine greater than methoxamine greater than clonidine greater than methyl norepinephrine. When the density of fat cells was reduced to less than 5 mg/ml, clonidine was a more effective inhibitor of isoproterenol-activated lipolysis thatn phenylephrine. Lipolysis that was activated by dibutyryl cyclic AMP, ACTH or cholera enterotoxin was not reduced by any alpha-adrenergic agent. Under conditions when clonidine failed to inhibit catecholamine-activated lipolysis (i.e., at cell densities greater than 15 mg/ml), it failed to antagonize the antilipolytic activity of phenylephrine. The antilipolytic activities of clonidine and phenylephrine were most effectively antagonized by the blocking drugs phentolamine and yohimbine; in contrast, phenoxybenzamine and prazosin were less effective blockers. These data indicate that the alpha-adrenergic receptor on hamster fat cells is similar to presynaptic alpha-adrenergic receptors. The data further suggest the possibility that phenylephrine may exert its action through a separate alpha-adrenergic receptor mechanism.

Adipose Tissue↗

Inhibition of cyclic AMP accumulation in hamster adipocytes with phosphatidic acid: differences and similarities with alpha adrenergic effects.

Clark et al (Journal of Cyclic Nucleotide Research 6:37 (1980)) demonstrated phosphatidic acid inhibition of cyclic AMP formation in WI-38 fibroblasts and suggested the hypothesis that cholinergic inhibition of adenylate cyclase is mediated through accumulation of this phospholipid. In view of these data, we tested the hypothesis that phosphatidic acid is involved in alpha-adrenergic inhibition of cyclic AMP formation in hamster adipocytes. The effects of phosphatidic acid on hormone and methyl xanthine stimulated cyclic AMP accumulation and lipolysis were studied. Phosphatidic acid inhibited 3-isobutyl-1-methyl xanthine (IBMX) stimulated cyclic AMP formation. The maximum inhibition (85% to 100%) of IBMX stimulated cyclic AMP accumulation was detected at 1.0 microM phosphatidic acid. When lipolysis was measured, however, inhibitory effects of phosphatidic acid were not evident until the concentration of phospholipid was increased to 300 microM. The cyclic AMP lowering and antilipolytic effects were detected using egg yolk phosphatidic acid, dipalmitoyl phosphatidic acid, dimyristoyl phosphatidic acid, distearoyl phosphatidic acid and palmitoyl lysophosphatidic acid but not with phosphatidylinositol, phosphatidylserine, phosphatidylethanolamine, phosphatidylcholine or 1,2- diglyceride. In contrast to phosphatidic acid, clonidine or N6-phenylisopropyl adenosine inhibited lipolysis in concert with inhibition of methyl xanthine stimulated cyclic AMP accumulation. Cyclic AMP accumulation increased by isoproterenol in combination with IBMX was partially blocked by clonidine but not by phosphatidic acid. These results show similarities as well as differences between clonidine and phosphatidic acid actions on hamster fat cells and do not, therefore, provide unequivocal support for the possibility that phosphatidic acid is intimately involved in alpha-adrenergic effects on hamster adipocytes. However, the high selectivity of phosphatidic acid suggests a physiological role of this agent in regulation of adenylate cyclase.

1-Methyl-3-isobutylxanthine↗

Activation of adenosine 3',5'-monophosphate-dependent protein kinase and its relationship to cyclic AMP and lipolysis in hamster adipose tissue.

The interrelationships among cAMP-dependent protein kinase activity, lipolysis, and cellular concentrations of cAMP were investigated in hamster epididymal adipose tissue. Isoproterenol, norepinephrine, and theophylline increased the protein kinase activity assayed in tissue extracts with no added cAMP, but not in the presence of added cyclic nucleotide. The maximum rate of lipolysis was associated with a nearly three-fold increase in cAMP levels and a protein kinase activity ratio of 0.8 (the ratio of activity assayed without cAMP to that assayed with cAMP). Rates of lipolysis less than maximum were associated with lesser degrees of protein kinase activity and lower levels of cAMP. The relatively pure alpha-adrenergic agent phenylephrine partially suppressed the isoproterenol-stimulated protein kinase activity, lipolysis, and cAMP levels. Conversely, the alpha-adrenergic blocking agent phentolamine increased the activity of protein kinase and cAMP levels in adipose tissues exposed to norepinephrine. These data are consistent with the primary role for cAMP and its dependent protein kinase in control of lipolysis in adipose tissue. Moreover, our data are consistent with the view that the antilipolytic action of alpha-adrenergic agents is mediated by a decrease in activity of protein kinase, caused by a decrease in cellular cAMP concentrations.

Adipose Tissue↗

Recurring intracranial meningiomas. Morphometrical evaluation of nuclear pleomorphism by S.A.M. (shape analytical morphometry) system.

Meningiomas are the most common neoplasms of the central nervous system and their biological behavior is not always predictable from the histologic appearance of the tumors. The nuclear pleomorphism seems to be one of the most important morphological features in the prediction of recurrence. By using analytical morphometric methods it is possible to quantify nuclear atypias and to obtain parameters describing nuclear contour irregularities and distortions of the figure. Moreover the amount of information obtained from analytical procedure allowed to discriminate, by multivariate discriminant analysis recurrent or no-recurrent meningiomas (5% of error).

Cell Nucleus↗