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Biomedical subjects

L Todorov

Publications and source records attributed to L Todorov.

8 recordsLinked to original sources
PubMed1996

Direct measurement of the release of ATP and its major metabolites from the nerve fibres of the guinea-pig taenia coli.

1. The release of adenosine triphosphate (ATP), adenosine diphosphate, adenosine monophosphate and adenosine from guinea-pig taenia coli in response to electrical stimulation of intramural nerves was measured directly using high performance liquid chromatography separation and fluorometric detection. 2. Purines were released in a frequency-dependent manner by trains of transmural electrical pulses at 1-30 Hz. 3. Electrically evoked release of ATP was abolished by tetrodotoxin (10(-6)mol/L) but was not affected by nicardipine (10(-6)mol/L). 4. The release of purines was reduced in the presence of atropine. 5. Pituitary adenylyl cyclase-activating peptide did not evoke the release of any purines and did not modify the electrically evoked release of purines. 6. The results suggest that ATP and its major metabolites are released from a neuronal source, possibly the enteric inhibitory nerves, in the guinea-pig taenia coli.

Adenosine↗
PubMed1991

Prejunctional nicotinic receptors involved in facilitation of stimulation-evoked noradrenaline release from the vas deferens of the guinea-pig.

In guinea-pig prostatic vas deferens loaded with [3H]-noradrenaline ([3H]-NA), nicotinic receptor agonists, nicotine and dimethylphenylpiperazinium (DMPP) enhanced the resting and facilitated the stimulation-evoked release of [3H]-NA in a concentration-dependent fashion. The effect of nicotine on both contraction of vas deferens and release of NA in response to field stimulation was stereospecific in favour of the naturally occurring (-)-enantiomer. Prolonged (15 min) exposure to (-)-nicotine resulted in a cessation of the facilitatory effect on NA release and on responses of the vas deferens to field stimulation. 2 The rank order of agonist potency in facilitating NA release was DMPP = (-)-nicotine greater than (+)-nicotine. Cytisine had no agonistic activity. The dissociation constants (KD) of antagonists were 9.3 +/- 0.6 and 31.4 +/- 2.4 microM for (+)-tubocurarine and hexamethonium, respectively, when (-)-nicotine was used as agonist. alpha-Bungarotoxin had no antagonistic activity. These findings suggest that nicotinic receptors located on noradrenergic axon terminals are different from those located postsynaptically in striated muscle or ganglia but seem similar to those present on cholinergic axon terminals at the neuromuscular junction. 3. Cotinine, the breakdown product of nicotine failed to have any agonistic activity indicating that nicotine itself is responsible for the effects observed on axon terminals. 4 Stimulation of presynaptic muscarinic receptors by oxotremorine prevented the nicotine-induced facilitation of [3H]-NA release, indicating the presence of both inhibitory muscarinic and facilitatory nicotinic receptors on noradrenergic axon terminals.

Animals↗
PubMed1991

[Gastrointestinal sphincters--pharmacologic viewpoints].

Bearing in mind the specificity of the functions of the gastrointestinal sphincters (GIS), we studied the responses of the lower esophageal sphincter (LES), the pyloric sphincter (PS), the ileocecal sphincter (ICS) and the internal anal sphincter (IAS) to noradrenaline (NA), acetylcholine (ACh), PGE1, PGF2 alpha and the peptide bombesin (B). The electrical and contractile activities as well as the response to field electrical stimulation (FES) were recorded. All sphincters except for PS responded to NA with depolarization and contractions. ACh at concentrations higher than 5 x 10(-6)M elicited a biphasic response from LES: depolarization followed by hyperpolarization and respectively contractions and relaxation. At concentrations higher than 10(-6)M ACh produced hyperpolarization and relaxation in IAS. Data were obtained about the modulating role of presynaptic N-cholinoreceptors in the release of a non-adrenergic, non-cholinergic (NANC) inhibitory neurotransmitter leading to hyperpolarization and relaxation in LES and IAS under the effect of exogenous ACh. PGE1 and PGF2 alpha increased the tone and decreased the FES-induced relaxation in LES. In PS PGE1 evoked relaxation and completely inhibited the response to FES. The pharmacological analysis showed that PGs modulated not only the adrenergic and cholinergic but also the NANC neurotransmission. Evidence is presented concerning the role of bombesin in the adrenergic, cholinergic, and NANC neurotransmission in LES.

Acetylcholine↗
PubMed1984

Neurotransmitter interactions in smooth muscles from cat internal anal sphincter (in vitro experiments).

The contractile activity of strips (15 X 2 mm) isolated from cat internal anal sphincter (IAS) has been studied under isometric conditions. Noradrenaline (above 10(-10) mol/l) induces contraction of IAS, antagonized by phentolamine. Isoprenaline (10(-8)-10(-5) mol/l) has no effect on IAS. Acetylcholine and carbachol (above 10(-6) mol/l) result in relaxation of the IAS preparations, which is blocked only by simultaneous administration of atropin (10(-6) mol/l) and hexamethonium (10(-4) mol/l). The acetylcholine-induced relaxation is not influenced by guanetidine and reserpine, but it is antagonized by tetrodotoxin (TTX) (10(-7) g/ml). Nicotine (10(-6)-10(-4) mol/l) also causes IAS relaxation which is not influenced by atropin, being blocked by hexamethonium and antagonized by TTX. The IAS relaxation induced by acetylcholine and nicotine is not associated with adrenergic mechanisms; it is assumed to be the result of a release of noncholinergic, nonadrenergic inhibitory neurotransmitter by means of presynaptic postganglionic cholinergic receptors. Data are also presented concerning the release of noradrenaline through presynaptic N-cholinergic receptors, when nicotine and high acetylcholine concentrations are applied after treatment of the preparations with scorpion venom or after increasing the K+-concentration in the nutrient solution to 16-20 mmol/l. The complex neurotransmitter interactions at IAS level are discussed.

Anal Canal↗
PubMed1984

Modulation of the release of noradrenaline and of noncholinergic, nonadrenergic inhibitory neurotransmitter through presynaptic N-cholinergic receptors by means of depolarizing agents in cat internal anal sphincter.

The contractile activity of smooth-muscle strips (15 X 2 mm), isolated from the internal anal sphincter [IAS] of chloralose-anaesthesized cats, was recorded under isometric conditions. The relaxation effects of exogenously applied acetylcholine (Ach) and nicotine (Ns on cat IAS turn into contractile after treatment of the preparations with depolarizing agent (increased [K+]0 scorpion venom, ouabaine). These contractile effects are blocked completely by phentolamine, guanetidine, hexamethonium and they are antagonized by TTX. Relatively high N concentrations induce a three-phase effect whose second contractile component is phentolamine- and guanethidine-sensitive. Field electrical stimulation (FES - 0.7-20 Hz, 0.1 ms, 40 V, duration 15 s) induces biphasic response in IAS: initial contraction which increases after an increase in [K+]0 and is blocked by phentolamine and guanethidine, with subsequent relaxation which is not affected by adrenergic and cholinergic blockers. The effects of FES are TTX-sensitive. The article discusses the problem of the release of noncholinergic nonadrenergic inhibitory neurotransmitter and of noradrenaline by means of presynaptic N-cholinergic receptors. It is assumed that the correlation in which the two transmitters are released depends on the different threshold value of the membrane potential of the nerve terminals, whereby excitatory-secretion coupling takes place.

Acetylcholine↗
PubMed1980

[Physical and physiological bases of rheography of the gastrointestinal tract].

In vitro experiments have shown that two kinds of factors are involved in the mechanism, by which the rheogram of the contractile activity of the gastro-intestinal organs is obtained: changes in the geometric parameters of the organ and its wall, on the one hand, and variations in tissue conduction, displayed during the contraction cycle in the smooth muscle, on the other.

Animals↗