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Biomedical subjects

D D Brănişteanu

Publications and source records attributed to D D Brănişteanu.

At least 19 recordsLinked to original sources
PubMed1992

Effects of activators and inhibitors of protein kinase A on increases in quantal size at the frog neuromuscular junction.

Adrenaline, permeable cyclic adenosine monophosphate (cAMP) derivatives and insulin are known to elicit an increase in quantal size at the frog neuromuscular junction, primarily by increasing the amount of acetylcholine (ACh) per quantum. The quantal size increases produced by adrenaline or cAMP were antagonized by the protein kinase inhibitor H8 N-[2-(methylamino)ethyl]-5-isoquinolonesulfonamide. The increase in quantal size produced by insulin was not prevented by H8. Quantal size is also increased by pretreatment in hypertonic solution; this increase was also antagonized by H8. The H8 did not alter the increase in miniature endplate potential (MEPP) frequency produced by the hypertonic solution. A permeable cGMP derivative had no effect on quantal size. The diastereomer (Sp)-cAMPS (cyclic 3',5'-phosphothoate) activates protein kinase A(PKA). It elicited an increase in quantal size. The (Rp)-cAMPS isomer is known to inhibit PKA; it had no effect on quantal size. The increase in quantal size produced by hypertonic solution was antagonized by (Rp)-cAMPS but not by (Sp)-cAMPS. Brief exposure to a hypertonic solution containing a phosphodiesterase inhibitor followed by incubation in the inhibitor leads to an increase in quantal size. We conclude that one pathway for signaling for an increase in quantal size involves activation of PKA and that hypertonic pretreatment acts via this pathway.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Adenosine alters the vascular effects of a diacylglycerol analogue and polymyxin B.

Endothelium-denuded rat aorta rings were used to study the possible relationship between protein kinase C and the mechanism of adenosine-induced smooth muscle relaxation. Adenosine (5 x 10(-4) M) partially relaxed the aortic rings contracted by either a depolarising amount of KCl (4 x 10(-2) M) or activation of protein kinase C with 1-oleoyl-2-acetyl-sn-glycerol (10(-6) M). The same amount of adenosine blocked the further relaxation obtained in the presence of polymyxin B (5 x 10(-5) M), a protein kinase C blocking agent. These results suggest a possible interaction in vascular smooth muscle between adenosine and protein kinase C.

Adenosine↗
PubMed1989

Adenosine effects upon the spontaneous quantal transmitter release at the frog neuromuscular junction in the presence of protein kinase C-blocking and -activating agents.

This paper gives experimental evidence involving protein kinase C (PKC) in the inhibitory effects of adenosine (ADO) upon the spontaneous transmitter release at the frog neuromuscular junction. In the presence of two PKC inhibitors--polymyxin B (5 x 10(-6) mol/l) and H-7 (10(-5) mol/l), both adenosine (5 x 10(-5) mol/l) and its stable analogue 1-PIA (5 x 10(-8) mol/l), significantly increased the rate of the spontaneous release of acetylcholine quanta. Even when PKC was activated with OAG (5 x 10(-6) mol/l) or TPA (162 x 10(-9) mol/l) and quantal release was increased greatly, ADO still inhibited release. ADO deaminase increased the PKC-induced activation of the transmitter release significantly.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1988

Cyclic GMP and protein kinase G inhibit the quantal transmitter release induced by protein kinase C.

Protein kinase G inhibits the spontaneous release of acetylcholine quanta at the frog neuromuscular junction as shown by the effects of H-8, a G kinase blocking agent. Moreover, the permeant dibutyryl cGMP blocked the frequency increase obtained in the presence of protein kinase C activators (diacylglycerol and phorbol ester) while the cAMP activated protein kinase A did show only an additive effect.

Animals↗
PubMed1987

Trifluoperazine-sensitive activation of the spontaneous transmitter release at the frog motor endplates by low doses of procaine.

Low concentrations of procaine (10(-6)-5 X 10(-5) mol/l) induced a significant increase of the spontaneous quantal transmitter release in the neuromuscular junctions of the frog cutaneous pectoris nerve-muscle preparation. The frequency of miniature endplate potentials (mepps) was increased although their size slightly decreased probably on the account of a partial block of Na+-channels at the postsynaptic membrane. The activatory effect of pre-caine was not altered under experimental conditions known to change the Ca2+ fluxes across the nerve terminal membrane such as using a Ca2+-free Ringer, or a Ca2+-channel blocker (D600), a high K+ Ringer or, finally, a low Na+ Ringer. In the presence of caffeine no change of procaine-induced activation appeared. Trifluoperazine (TFP), in a concentration known to specifically block calmodulin, completely blocked the procaine-induced increase of mepp frequency. These data suggest that procaine presumably by way of a calmodulin-dependent mechanism is related to the free cytosolic Ca2+ equilibrium. It is possible that procaine increases the free cytosolic Ca2+ concentration by blocking an active calmodulin-dependent Ca2+ extrusion mechanism.

Acetylcholine↗
PubMed1979

Adenosine effects upon transmitter release parameters in the Mg2+-paralyzed neuro-muscular junction of frog.

The influence of adenosine upon the process of transmitter release was investigated in Mg2+-paralyzed frog neuromuscular junction by using conventional microelectrophysiological techniques and binomial statistical analysis. The statistical parameters used were: m (mean number of quanta released per impulse), p (the probability of quantal release) and n (store of quanta available for release). Adenosine decreased the mean quantal content (m) by reducing n. This effect appeared to be dependent upon the free intracellular Ca2+. The nucleoside competed with the transmitter releasing effects of ouabain and increased the amount of effective Ca2+ necessary for quantal release. It did not change the slope of release parameters modification during low-frequency facilitation. The data are discussed in terms of a physical model of release.

Adenosine↗
PubMed1979

Dual action of ouabain on transmitter release at neuromuscular junctions of the frog.

Ouabain increased both spontaneous and evoked transmitter release in Mg++-treated frog neuromuscular junctions. This action developed as a two-step process which affected both miniature end-plate potential (m.e.p.p.) frequency and the binomial distribution of e.p.p.s. During the first part of its action, which lasts for approximately 60 min, ouabain (10(-5) M) increased the m.e.p.p. frequency following a saturable process. The increase in m.e.p.p. frequency was blocked by tetrodotoxin (15 nM). The quantal parameters of release, m and n, showed a significant increase but the parameter p was unaffected. Since the same changes in the binomial parameters were observed in Mg++-treated junctions exposed to low [Na+]0 in the absence of ouabain, it can be concluded that Na+ concentration played an important role in the increase of transmitter release. After 60 min in ouabain (10(-5) M) m.e.p.p. frequency increased by an exponential process. The binomial parameters of transmitter release, m and p, increased while n remained unchanged. This action was not influenced by TTX pretreatment nor was it reproduced by decreasing [Na+]0. The mechanism responsible for this action seems to be the Ca++- releasing effect of ouabain from the cytoplasmic sequestering sites.

Action Potentials↗
PubMedDate not supplied

Barraquer-Simons syndrome. Report of a case and review of the literature.

Among lipodystrophies, the Barraquer-Simons syndrome or "parital lipodystrophy of the cephalothoracic type" is a rare condition of unknown origin characterized by a progressive atrophy of the subcutaneous fat of the upper part of the body. We report a 34-year-old woman with progressive loss of subcutaneous fat during 20 years, first affecting the face and spreading to the upper part of the body, equally presenting hypertrophy of the lower body fatty tissue. An overview of this rare syndrome is made.

Adipose Tissue↗
PubMedDate not supplied

[Thyroxine therapy in benign thyroid nodules].

Levothyroxine (LT4) treatment in benign thyroid nodules is a controversial management. The favorable response varies between 10-60%, being, in some studies, comparable between treated and untreated groups. The aim of this study was to evaluate the response of uninodular goiter at the LT4 treatment, in comparison with untreated patients. The study group (S) included 53 patients diagnosed with nodular goiter, treated with LT4 for 1 year. 26 patients with nodular goiter, age and sex-matched, untreated, constituted the control group (C). All patients were from a minor iodine deficient area. The including criteria were euthyroidism, single nodule, solid (ultrasonography), cold (Scintigraphy), and benign (FNAB). After 1 year mean nodular volume had a significant decrement in both groups, higher in group S (35%: from 7.8 to 5.2 mL, p = 0.0098) than in group C (25%: from 8.4 to 5.9 mL, p = 0.026). Linear regression showed a slight correlation between the nodular decrement and the initial volume (r = 0.23): the responders percentage was higher in nodules with a volume < 5 ml than in those with volume > 5 ml (51.5% vs o 19.6%, p < 0.0001). The evolution of treated nodules seamed to be better than of the untreated ones, but the differences were only slightly significant. We believe that the evolution of thyroid nodules under LT4 treatment can be influenced by the iodine supply, since in most of the studies from minor iodine deficiency regions (Europe, South America) the response is better than in regions with sufficient iodine supply (North America). Knowing the potential side effects of LT4 therapy, this kind of management of benign thyroid nodules should be reserved to selected cases.

Adult↗
PubMedDate not supplied

Short-time adenosine deaminase interventions upon underperfused rat hearts in vitro--a test for the role of adenosine in the coronary flow control.

Spontaneously beating rat heart Langendorff preparations, perfused with Tyrode solution under low flow conditions (1.62 +/- 0.47 ml/min at 55 mmHg), were used to investigate the role of adenosine in the coronary flow control, by means of adenosine-deaminase injections into the perfusion system. Adenosine deaminase did not influence the control coronary flow, but significantly reduced autoregulation, hypoxic vasodilation, reactive hyperemia and functional adrenaline-induced hyperemia. All these effects, excepting the hypoxic vasodilation reduction, dependent upon the moment of enzyme injection during the experiment. Under the mentioned conditions adenosine seems to be responsible for more than half of the autoregulation of the coronary flow. Adenosine deaminase completely abolished reactive hyperemia during control perfusion but only delayed it under adrenaline perfusion.

Adenosine↗
PubMedDate not supplied

Calmodulin and the transmitter release at the neuromuscular junction. Contradictory results obtained with trifluoperazine.

Calmodulin seems to be strongly involved in the process of transmitter release. By activating a specific proteinkinase system, calmodulin could initiate the phosphorylation of some axolemal or vesicular protein, thus triggering the exocytosis of the synaptic vesicles and the transmitter release. Under these conditions it was to be expected that a calmodulin blocking agent such as trifluoperazine, used in appropriate concentrations for this effect, should block the transmitter release. Contradictory results determined us to reexamine the question under extended experimental conditions. Our data suggest that calmodulin could both activate and block the transmitter release through probably different mechanisms.

Acetylcholine↗
PubMedDate not supplied

Some neural effects of adenosin.

The possible neural effects of adenosine were investigated by using electrophysiological techniques at the level of some central and peripheral synapses. The evoked potentials in the somatosensorial cerebral cortex are influenced according to both the type of administration and the level of the electrical stimulation. While the local application does not induce significant alterations, the intrathalamic injections and the perfusion of the IIIrd cerebral ventricle do change the distribution of activated units at the level of different cortical layers especially during the peripheral stimulation. The frequency of spontaneous miniature discharges intracellularly recorded in the neuromuscular junction (mepp) is significantly depressed by adenosine. This effect is calcium- and dose-dependent. The end plate potentials (EPP) were also depressed. The statistical binomial analysis of the phenomenon indicated that adenosine induces a decrease if the presynaptic pool of the available transmitter. The data obtained demonstrate a presynaptic inhibitory action of adenosine beside its known vascular and metaholic effects.

Adenosine↗
PubMedDate not supplied

Modulatory effects of adenosine upon the transmitter release in the hippocampal slice preparation of rats.

In the hippocampal slice preparation of rats, preloaded with 3H-glutamate a local perfusion technique was used in order to measure the labelled transmitter output. The electrical receptive stimulation of the Schaffer collateral-commissural projections resulted in a detectable 3H-glutamate release which was significantly increased in the presence of 4-aminopyridine (4-AP). Exogenous adenosine and its analogue L-PIA induced a slight unsignificant reduction of the release while in the presence of 4-AP the release was almost completely blocked. Adding adenosine deaminase (ADA) did not change the normal transmitter release while in the presence of 4-AP the elimination of the endogenous adenosine brought about a significantly higher 3H-glutamate output. It is concluded that the adenosine-induced presynaptic inhibition of the transmitter release could be a significant mechanism under conditions in which the synaptic activity is abnormally high. This effect seems to be mediated via the A1 adenosine receptor since the D-PIA isomer application has no significant inhibitory effects.

4-Aminopyridine↗