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Biomedical subjects

D Budai

Publications and source records attributed to D Budai.

31 records · Page 2Linked to original sources
PubMed1989

Endothelium removal does not affect potentiation by neuropeptide Y in rabbit ear artery.

Influence of endothelial cells on the effect of neuropeptide Y (NPY) was investigated. NPY (30 nM) doubled the vasoconstriction elicited by transmural nerve stimulation (8 pulses at 8 Hz) in the perfused rabbit ear artery with or without endothelium. Conditions that increase the biophase concentration of norepinephrine, longer stimulation trains or application of yohimbine, decreased the potentiation by NPY, although in the presence of cocaine potentiation by NPY was unchanged. However, no significant differences between control and endothelium-removed arteries were revealed. Thus modulation of adrenergic neurotransmission by NPY does not depend on endothelium-derived vasoactive substances.

Animals↗
PubMed1989

Changes in acetylcholine content, release and muscarinic receptors in rat hippocampus under cold stress.

The aim was to study the mechanism of the previously established decrease in acetylcholine (ACh) concentration in the rat hippocampus under cold stress. Male rats were exposed for 14 days to cold (5 degrees C) or kept (controls) at room temperature (24 degrees C). Acetylcholine content, release and muscarinic receptor binding were investigated in the hippocampus. Cold exposure resulted in a decrease of ACh concentration in the dorsal hippocampus. Moreover, the potassium-evoked release of ACh from hippocampal slices was increased and an increase of maximal binding capacity of [3H] (-) quinuclidinyl benzilate in the dorsal hippocampus of cold exposed animals was also observed. Thus the decrease of hippocampal ACh concentration under cold exposure is probably due to its increased release. On balance then, our results demonstrate that cold stress in the rat induces significant activation of the hippocampal cholinergic system.

Acetylcholine↗
PubMed1989

Opioid-induced prejunctional inhibition of vasoconstriction in the rabbit ear artery: alpha-2 adrenoceptor activation and external calcium.

Inhibition of norepinephrine release by opioid agonists is inversely related to the stimulation train length. The possible interaction between activation of prejunctional alpha-2 adrenergic receptors and the release-inhibiting opioid receptors as well as the effect of changes in Ca++ entry into adrenergic varicosities during repetitive stimulation were investigated by recording vasoconstriction of the rabbit ear artery perfused in vitro. Neither the activation of the alpha-2 adrenoceptor-mediated negative feedback by clonidine nor its inhibition by yohimbine altered the neuroinhibitory potency for dynorphin 1-13 or Met-enkephalin at any stimulus train length. Experimental conditions known to increase the entry of calcium into the varicosities mimicked the effect of the increase in the stimulation train length on the modulation of norepinephrine release by opioids. Increasing the extracellular calcium concentration (from 1.6-5 or 8 mM) diminished the inhibitory effect of opioids and tended to abolish the dependence on stimulation train length. Conversely, lowering the calcium concentration (from 1.6-1 mM) increased the inhibition by opioids and enhanced the dependence on train length. These results do not suggest a direct interaction between activation of opioid receptors and alpha-2 adrenoceptors. Rather, they indicate the role of opioid receptor activation in a primary modulation of Ca++ influx which becomes masked by the high levels of axoplasmic calcium which are achieved during a continued stimulation train.

Animals↗
PubMed1989

Neuropeptide Y preferentially potentiates responses to adrenergic nerve stimulation by increasing rate of contraction.

Neuropeptide Y (NPY) is colocalized with norepinephrine and coreleased from adrenergic nerves. NPY reportedly can influence vascular neuroeffector transmission in both negative and positive directions. Mechanisms by which NPY effects are exerted and their relative contribution may vary between different blood vessels. Therefore, we investigated effects of NPY on adrenergic neurotransmission in ring segments of the rat tail artery by measuring isometric force development and [3H]norepinephrine release. NPY (1-100 nM) potentiated responses to transmural nerve stimulation (3 Hz, six pulses) by more than 300% but produced no direct contractile effects. NPY potentiated responses to longer transmural nerve stimulation trains (30-100 pulses) or to exogenous norepinephrine by only 30%. NPY had no effect on [3H]norepinephrine overflow with either short (six pulses) or long (30 pulses) stimulation trains. Contractile responses to transmural nerve stimulation were completely blocked by prazosin (10(-7) M) both in the absence and presence of NPY. Since the impact of an increased rate of contraction on the contractile response achieved would be greater with short stimulation trains, the effect of NPY on contraction rate was analyzed. NPY increased the rate of contraction to both norepinephrine and transmural nerve stimulation. It is hypothesized that NPY increases the early (phasic) component of the contractile response by preferentially influencing release of intracellular calcium stores. These findings suggest that the effects of NPY will be more profound on phasic rather than sustained patterns of nerve traffic.

Animals↗
PubMed1989

Prejunctional inhibitory effect of a dopamine D-2 agonist, N-0437, on vascular adrenergic responses.

N-0437 [2-(N-propyl-N-2-thienylethylamino)-5-hydroxytetralin], a potent and selective agonist for D-2 dopamine receptors, was used to investigate inhibitory prejunctional dopamine receptors in the rat tail artery and rabbit ear artery. N-0437 inhibited contractile responses to transmural nerve stimulation in a frequency dependent manner. Thus, N-0437 profoundly inhibited responses to nerve stimulation in the rat tail artery at a frequency of 1 Hz (ED50 = 1.6 nM), but had minimal effects when nerves were stimulated at 6 Hz. The D-1/D-2 dopamine agonist, apomorphine, exhibited a similar frequency dependent inhibitory effect but with less potency (ED50 = 30 nM at 1 Hz). In concentrations up to 1 microM, N-0437 had no effect on responses to exogenously applied norepinephrine, but N-0437 inhibited [3H] norepinephrine efflux induced by transmural stimulation. Inhibitory effects of N-0437 were blocked by the D-2 antagonist sulpiride but not by the D-1 antagonist SCH 23390. Furthermore, the selective D-1 agonist SKF 38393 did not inhibit vascular responses to adrenergic nerve stimulation. These data indicate that the inhibitory effects of N-0437 are via activation of D-2 dopamine receptors that inhibit norepinephrine release. Thus, N-0437 shows potency and selectivity of action for prejunctional D-2 dopamine receptors in vascular tissues. The frequency dependence of the actions of N-0437 suggest that the level of sympathetic activity is an important variable in determining effectiveness of prejunctional modulation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Influence of stimulation train length on the opioid-induced inhibition of norepinephrine release in the rabbit ear artery.

In perfused segments of rabbit ear artery the effects of opioid agonists on vasoconstrictor responses to adrenergic nerve stimulation and stimulation-evoked [3H]norepinephrine overflow were compared using trains of 8, 40 or 120 monophasic pulses at 8 Hz with 1 msec duration and 40 V amplitude. Both delta selective peptides, [D-Ala2, D-Leu5]-enkephalin, met-enkephalin and leu-enkephalin, and preferential kappa ligands, dynorphin1-13 and ethylketocyclazocine, significantly reduced the vasoconstriction evoked by 8 pulses at 8 Hz. The magnitude of this effect was inversely related to the stimulus train length. In most cases, opioid agonists were highly effective with short stimulus trains, but failed to decrease vasoconstrictor responses by more than 10 to 15% with trains of 120 pulses at 8 Hz. In good correlation with these data, in tissue preincubated with [3H]norepinephrine the inhibitory effect of opioids on the tritium overflow evoked by 8 or 120 pulses at 8 Hz was inversely proportional to the length of stimulation. Our findings confirm that opioid agonists interact with a heterogeneous prejunctional receptor population to modulate the action potential-evoked release of norepinephrine in the isolated ear artery of the rabbit. This modulation is more pronounced at the beginning of a stimulus train when the negative feedback inhibition of norepinephrine release is still not fully operative. It is suggested that the physiological role of opioid peptides could be more significant during a short rather than a prolonged vasoconstriction.

Animals↗
PubMed1987

Acetylcholine and its enzymes in some brain areas of the rat under stress.

A period of 1 or 24 h of cold stress (5 degrees C) resulted in a significant decrease of acetylcholine (ACh) concentration in the hypothalamus and hippocampus in rats. In the hippocampus the activity of the choline acetyltransferase (ChAT) was significantly increased after 24 h and that of acetylcholinesterase (AChE) after 1 and 24 h exposure to cold, whereas in the hypothalamus, AChE activity was found to be decreased, albeit only after 24 h exposure. Separate investigation of the dorsal and ventral hippocampus under 24 h of cold revealed that the ACh decreased in the dorsal hippocampus only, where no change in ChAT activity was observed. On the other hand, ACh showed no change in the ventral hippocampus where an increase of ChAT activity was found. Forced swimming for 20 min also induced a significant decrease of ACh in the hippocampus and cerebral cortex, along with a significant increase of choline concentration in the given regions. We conclude that under certain stress situations the cholinergic system in rat brain areas, mainly in the hippocampus and hypothalamus, is activated.

Acetylcholine↗
PubMed1987

Effects of trifluoperazine on the cholinergic function of the hippocampus of the rat.

The changes induced in the level and turnover rate (TRACh) of acetylcholine (ACh) in the hippocampus and in the in vitro release of [3H]ACh by intracerebroventricular injection of trifluoperazine (TFP) were studied. Rats were killed by microwave irradiation at various times after treatment with drug or vehicle and the levels of ACh were measured by gas chromatography. After the administration of 100 micrograms trifluoperazine, the content of ACh of the whole hippocampus increased from 24.0 +/- 2.9 to 35.2 +/- 4.2 nmols/g wet weight over a 60 min period, while the turnover rate was markedly decreased (from 0.86 to 0.53 nmols/min/g wet tissue weight). The potassium-evoked release of [3H]ACh from slices of hippocampus under in vitro conditions was decreased in a concentration-dependent manner by preincubation with 50 and 100 microM of trifluoperazine for 60 min. The results support the assumption that trifluoperazine can alter neurotransmission, possibly by inhibiting the calcium-binding protein calmodulin, and/or by interfering with cell metabolism.

Acetylcholine↗
PubMed1986

Isolation of choline and choline esters from Krebs-Ringer solution for gas chromatographic determination.

A simple and efficient novel method for isolating picomole amounts of choline and choline esters in milliliter volumes of Krebs-Ringer solution has been developed. The procedure is based on the observation that the solubility of choline esters in acetonitrile is 10(4)-10(5) times higher than that of the inorganic salt constituents of Krebs-Ringer solution. The glucose content of the medium, which prevented the one-step isolation of choline esters based on acetonitrile extraction from its lyophilizate, was removed using Amberlite CG-50 column chromatography. Bound compounds to the column were eluted in 0.25 N HCl and lyophilized. The lyophilizate was extracted with acetonitrile, which was then decanted and eliminated by evaporation to dryness. The resultant glucose and salt-free residue can be assayed by gas chromatography. Total recoveries of added choline and choline esters over the entire isolation procedure, measured isotopically and/or gas chromatographically, were 93 and 97%, respectively. Due to the high and close-to-equal recoveries of choline esters, and the high purity of the final product, this procedure is suitable for estimating acetylcholine and choline in neural tissue perfusates by gas chromatography, as was demonstrated by this method using hippocampal slices.

Acetonitriles↗
PubMed1986

4-(1-Naphthylvinyl)pyridine decreases brain acetylcholine in vivo, but does not alter the level of acetyl-CoA.

The effects of intraperitoneally administered 4-(1-naphthylvinyl)pyridine (NVP; 200 mg/kg) on the concentrations of acetylcholine (ACh), choline (Ch), and acetyl-CoA (AcCoA) in rat striatum, cortex, hippocampus, and cerebellum were investigated. Twenty minutes after treatment, the content of ACh was significantly diminished, whereas that of Ch was increased. In response to stress (swimming for 20 min), these changes were enhanced. However, the AcCoA content did not change in any of the brain regions. It is thus very likely that the decrease of brain ACh concentration induced by NVP is due to the drug's effect on choline acetyltransferase (ChAT) and/or the reduction of the high-affinity Ch uptake, and not on the availability of AcCoA. Presumably, the pharmacologically diminished activity of ChAT may become the rate-limiting factor in the maintenance of ACh levels in cholinergic neurons.

Acetyl Coenzyme A↗
PubMed1984

In vivo effects of beta-bungarotoxin on the acetylcholine system in different brain areas of the rat.

The in vivo effects of beta-bungarotoxin (beta-BT) on the acetylcholine (ACh) system were studied in the whole cerebrum and in different brain regions. The effect of beta-BT on cerebral ACh and choline (Ch) contents was time-dependent. The results show that a single intracerebroventricular injection of 1 microgram toxin increased both the ACh and Ch contents in the cortex, hippocampus, and cerebellum, while in the striatum the ACh level was decreased. Ten nanograms of toxin injected into the lateral ventricle twice, on the first and third days, led to a reduced ACh level 2 days after the last treatment. In animals treated with the same dose three times, on the first, third, and fifth days, and sacrificed 2 days after the last injection, the choline acetyltransferase and acetylcholinesterase activities were reduced and the number of muscarinic acetylcholine receptors was decreased. A biphasic effect of the toxin was therefore demonstrated. It is suggested that in the first phase of the toxin effect the increased levels of ACh and Ch may be due to the inhibition of neuronal transmission, while in the second phase, when the elements of the ACh system are reduced, the neuronal degenerating effect of beta-BT plays a significant role.

Acetylcholine↗
PubMed1983

Modification of bursting in a Helix neuron by drugs influencing intracellular regulation of calcium level.

The effect of ruthenium red, caffein and EGTA (ethyleneglycol tetraacetic acid) influencing intracellular Ca2+ level as well as that of pH-lowering was investigated on identified RPal neuron of Helix pomatia characterized by bimodal pacemaker (bursting) activity. Drugs were applied both extracellularly and intracellularly. Intracellular injection was performed from micropipettes by pressure. It was found that intracellular injection of ruthenium red, caffein, EGTA and pH-lowering caused immediate short hyperpolarization and suspension of bursting. The effect of caffein and lowering of pH was biphasic, hyperpolarization was followed by an increase of spiking. Following EGTA injection the amplitudes of interburst hyperpolarizing waves decreased, and prolongation of spikes occurred. Extracellular application of ruthenium red caused slight depolarization, while caffein produced mainly effects that were similar to those of the intracellular injection. Adding EGTA into the bath resulted in cessation of bursting, and later on also spike generation was blocked. All these effects could be eliminated by washing. It is concluded that Ca-influx during spiking cannot be considered as a single factor in maintaining bursting activity, nevertheless, intracellular binding and liberation of Ca depending on the cell metabolism should also be taken into consideration as a possible mechanism of burst regulation.

Animals↗