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Biomedical subjects

A De Luca

Publications and source records attributed to A De Luca.

At least 253 records · Page 14Linked to original sources
PubMed1990

Changes in membrane ionic conductances and excitability characteristics of rat skeletal muscle during aging.

Membrane electrical properties, component ionic conductances and excitability characteristics of extensor digitorum longus muscle from 3-4, 16 and 29 months old rats were measured "in vitro". Fiber diameter, membrane resistance (Rm) and membrane capacitance, increased with aging, and the increase was significant at 29 months. The increase of Rm was mostly due to a decrease of chloride conductance (GC1), whereas potassium conductance (GK) increased only slightly, at 16 and 29 months. Due to the lowered GC1, the latency of action potential increased at both ages with a consequent prolongation of the duration of action potential. Nevertheless, a decrease in the firing capability was recorded in the aged fibers. Our results indicate, that during aging, the most affected parameter of skeletal muscle fibers is GC1, although changes of this passive conductance alone cannot entirely account for the changes in the excitability characteristics recorded.

Aging↗
PubMed1990

Responses of rat isolated intestinal segments to stimulation of perivascular mesenteric nerve fibres.

1. Isolated preparations of segments of rat jejunum were set up for isotonic recording of the activity of the longitudinal smooth muscle and the extrinsic nerve supply running with the mesenteric blood vessels was stimulated for 30-s periods at 0.5-20 Hz. 2. Contractions were regularly elicited during periods of stimulation at 0.5-2 Hz, and were usually elicited during stimulation at 5 Hz, but relaxations were usually elicited during stimulation at 10 and 20 Hz. On cessation of the period of stimulation, a secondary contraction occurred in most preparations regardless of whether the primary response during the period of stimulation had been a contraction or a relaxation. 3. Tetrodotoxin (0.9 microM) abolished responses during periods of stimulation and the secondary contraction. 4. The relaxations were mimicked by noradrenaline and were abolished by blockade of alpha- plus beta-adrenoceptors but were not affected by hexamethonium, indicating that they are attributable to stimulation of postganglionic noradrenergic fibres. 5. The contractions were mimicked by acetylcholine and were abolished by atropine and hexamethonium, suggesting that they are attributable to stimulation of preganglionic cholinergic nerves: they were also abolished in the presence of capsaicin, indicating that sensory neuropeptide-containing nerve fibres may be involved. 6. The secondary contraction that usually occurred on cessation of stimulation was still present after blockade by atropine or capsaicin of the contractions occurring during stimulation. It was also present after blockade by propranolol and phentolamine of the relaxations occurring during stimulation, and was not affected by indomethacin.

Animals↗
PubMed1990

Effects of omega-conotoxin GVIA on autonomic neuroeffector transmission in various tissues.

1. The effects of omega-conotoxin GVIA (conotoxin), a potent inhibitor of neuronal N-type Ca2+ channels, have been examined on responses to stimulation of noradrenergic, cholinergic and non-adrenergic, non-cholinergic (NANC) nerves in a range of isolated tissues to investigate the role of conotoxin-sensitive Ca2+ channels in neurotransmission. 2. Contractions elicited by field stimulation of noradrenergic nerves in rat and mouse anococcygeus muscles, rabbit ear artery and rat vas deferens (epididymal portion) were inhibited by conotoxin. Responses to noradrenaline, and to adenosine triphosphate in the vas deferens, were not affected. 3. Positive chronotropic responses to field stimulation of noradrenergic nerves were inhibited by conotoxin in rat and mouse atria, but responses to noradrenaline and tyramine were not affected. 4. The stimulation-induced release of noradrenaline was inhibited by conotoxin in the rabbit ear artery and in rat and mouse atria. 5. Relaxations in response to stimulation of the noradrenergic perivascular mesenteric nerves were reduced or abolished by conotoxin in rat and rabbit jejunum. The response to noradrenaline in rat jejunum was not affected. 6. Contractions elicited by stimulation of cholinergic nerves were inhibited by conotoxin in rat jejunum and mouse ileum (perivascular mesenteric nerves), and in guinea-pig taenia caeci (field stimulation). Responses to acetylcholine in rat jejunum and mouse ileum were not affected. 7. Contractions elicited by stimulation of the cholinergic plus NANC pelvic nerves were inhibited by conotoxin in rabbit colon, and to a lesser extent in guinea-pig colon. The stimulation-induced contraction of the guinea-pig colon was inhibited by conotoxin by a greater proportion in the presence than in the absence of atropine. Responses to acetylcholine were not affected in the rabbit colon but were slightly reduced in the guinea-pig colon. 8. Relaxations in response to field stimulation of NANC nerves were inhibited by conotoxin in guinea-pig taenia caeci and rat gastric fundus strips, and in rat anococcygeus muscle when the tone was raised by guanethidine but not when it was raised by carbachol. The relaxations produced by sodium nitroprusside in the rat gastric fundus and anococcygeus were not affected. 9. Contractions of the rat bladder elicited by stimulation of the peri-urethral nerves, which are NANC- and cholinergically mediated, were relatively insensitive to inhibition by conotoxin. The response were almost completely abolished by tetrodotoxin. 10. The conotoxin-induced inhibitions of responses to nerve stimulation developed slowly and persisted after removal of conotoxin. The responses were almost completely abolished by tetrodotoxin. 10. The conotoxin-induced inhibitions of responses to nerve stimulation developed slowly and persisted after removal of conotoxin. 11. The inhibitory effect of conotoxin was inversely proportional to the frequency of stimulation (in several preparations) and to the Ca2+ concentration in the bathing solution (in rat vas deferens). These observations suggest that the inhibition by conotoxin of the Ca2+ influx required for excitation-secretion coupling in autonomic nerve terminals is not absolute, and can be overcome by repeated stimulation or by raising the Ca2 + concentration.

Animals↗
PubMed1989

The effects of taurine on pharmacologically induced myotonia.

Taurine reduces the excitability of striated muscle fibers by increasing the membrane conductance to chloride ions (GCl). This action was tested on rats made myotonic by drugs that block GCl by different mechanisms. Experiments were made "in vivo" using electromyographic (EMG) recordings and "in vitro" with intracellular microelectrode recordings from extensor digitorum longus muscle fibers. Taurine did not antagonize the myotonic discharges produced in vivo by anthracene-9-carboxylic acid, nor did it restore GCl lowered in vitro by this agent. However, when myotonia was chronically induced by 20,25 diazacholesterol, taurine given chronically in vivo or acutely in vitro antagonized the EMG myotonia as well as the reduced GCl and increased excitability of single fibers. We conclude that taurine acts directly on chloride channels to modify their kinetics. Our findings suggest that further clinical studies on the use of taurine in muscle disease involving abnormal excitability or chloride channel function will be useful.

Animals↗
PubMed1989

Membrane ionic conductances in normal and denervated skeletal muscle of the rat during development.

The development of membrane ionic conductances of rat extensor digitorum longus (EDL) muscle fibers was studied in vitro using intracellular recordings. At 7-8 days after birth, the potassium conductance (GK) dominated the total membrane conductance while the chloride conductance (GCl) was very low. A rapid increase of GCl towards adult values was observed after few days (12-14 day old rats), whereas GK did not decrease up to day 23. Denervation at 7-8 days after birth suppressed the maturation of the electrical parameters measured, and 15 days after the nerve crush, GCl was just detectable. These results suggest that the maturation of the electrical properties, and in particular that of the resting chloride conductance in mammalian striated muscle fibers, occurs during the first weeks of postnatal life and is dependent on innervation.

Animals↗
PubMed1989

The effect of diphenylamine-2-carboxylate on C1- channel conductance and on excitability characteristics of rat skeletal muscle.

The effect of diphenylamine-2-carboxylate (DPC), a blocker of the C1- conductive pathway in C1- transporting epithelia, has been evaluated in-vitro on the electrophysiological variables of rat extensor digitorum longus muscle fibres. DPC (5-240 microM) caused a dose-related increase of membrane resistance which was attributed entirely to a fall in C1- channel conductance (IC50, 120 microM), since potassium conductance was not affected by the treatment. DPC also modified fibre excitability. A significant dose-dependent increase was observed in the latency of the action potential and in the excitability of the membrane. DPC was less potent on striated fibres than anthracene-9-carboxylic acid, another specific blocker of C1- channel conductance. Moreover DPC was less potent on skeletal muscle than on C1- transporting epithelia. Morphological differences in the C1- channels or of the drug binding sites may account for the differences between tissues.

Animals↗
PubMed1988

Involvement of alpha 1-adrenoceptors in chronotropic responses to endogenously released amines in the pithed rat.

1. In pithed rats, yohimbine (1 mg/kg i.v.) enhanced the positive chronotropic responses to spinal stimulation of cardiac sympathetic nerves with eight pulses delivered at 2 or 4 Hz, indicating that auto-inhibition was operating, but did not increase responses to shorter lengths of trains of 8 pulses at 8, 16 or 32 Hz which did not allow sufficient time for auto-inhibition to come into effect. 2. The positive chronotropic response to cardiac sympathetic nerve stimulation with eight pulses at 8 Hz of about 60 beats/min was not affected by prazosin (1 mg/kg) or diltiazem (0.2 mg/kg), but was reduced to about 20% of the control value by propranolol (1 mg/kg). 3. In the presence of propranolol, the residual positive chronotropic responses to cardiac sympathetic nerve stimulation were virtually abolished by prazosin (1 mg/kg) or diltiazem (0.2 mg/kg). 4. The positive chronotropic response to tyramine (0.1 mg/kg i.v.) was reduced from 100 to 12 beats/min by propranolol (1 mg/kg), and the residual response was abolished by prazosin. 5. The findings indicate that noradrenaline released from cardiac sympathetic terminals by nerve stimulation or by tyramine acts on alpha 1-adrenoceptors to produce a positive chronotropic response that is revealed when beta-adrenoceptors are blocked.

Animals↗
PubMed1988

The influence of activation or inhibition of protein kinase C on the release of radioactivity from rat isolated atria labelled with [3H]-noradrenaline.

1. The release of radioactivity from rat isolated atria preloaded with [3H]-noradrenaline ([3H]-NA) evoked by electrical field stimulation (2 Hz, 1 ms, 60 s) of intraneuronal sympathetic nerves, high potassium (64.7 mM) or tyramine (0.3 micron) was used as an index of noradrenaline release. 2. Activation of protein kinase C by phorbol 12-myristate 13-acetate (PMA) produced a concentration-dependent enhancement of field stimulation-induced outflow of radioactivity, whereas polymyxin B, an inhibitor of protein kinase C, reduced [3H]-NA release evoked by field stimulation. The enhancement observed in the presence of PMA was attenuated by polymyxin B (10 and 70 microns). 3. Release of noradrenaline evoked by membrane depolarization in a high potassium medium was similarly affected by PMA and polymyxin B. 4. In contrast, the release of noradrenaline evoked by the indirectly acting sympathomimetic amine, tyramine, was not altered by PMA. Polymyxin B in a concentration of 70 microns, but not 10 microns caused a slight reduction in tyramine-induced outflow of radioactivity. 5. The spontaneous outflow of radioactive compounds was not affected by either PMA or polymyxin B in the bathing medium. 6. The findings suggest that protein kinase C may play a role in the exocytotic release of noradrenaline but not in the displacement of noradrenaline by indirectly acting sympathomimetic amines.

Animals↗
PubMed1984

[Anti-thirst action of propranolol].

A reduction of the thirst was observed one hour after intramuscolar injection of 0.3 mg/kg propranolol in the rat; this effect was not observed with higher doses. According to work hypotheses, small doses could act blocking renal beta-adrenergic receptors: the stopped renin emission reduces angiotensin production that is the basic factor of thirst. The AA hypothesize that the lack of the effect in response to higher doses of propranolol can be explained through a different action of this drug which antagonizes the first one.

Animals↗
PubMed1984

[Mechanogram profile of the guinea pig intestine. The supertone].

The authors detected the possibility, during the phase of low tone contraction of isolated intestine, to develop a further contraction, a supertone (S), simply washing the preparation. It has been evidenced that S appears when the tonic phase is low; it does not disappear if the tone is increased lowering NaCl concentration in the saline plasma; is absent in the KCl induced contraction; is induced also by low doses of atropine; is decreased by digitalic agents. The results obtained lead the authors to conclude that: the reduced tonic phase is due to a positive factor, the Ca++ of the cytoplasm, and to a negative factor, the high level of cytoplasmic Na+. This high level of Na+ is maintained by a dynamic equilibrium with ion input through channels opened by muscarinic agent and output by a Na-K-ATP asi pump. The Na+ output is predominant and fraction of Ca++, no longer counterbalanced by Na+, causes the rise of S.

Animals↗