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  • 1
    Electronic Resource
    Electronic Resource
    Evidence for bilateral vagal innervation of postganglionic parasympathetic neurons in chicken heart (1983)
    Springer
    Journal of neural transmission 56 (1983), S. 239-247 
    Details
    ISSN: 1435-1463
    Keywords: Parasympathetic nervous system ; acetylcholine ; heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Stimulation of the cervical vagus nerves caused an output of acetylcholine (ACh) from the isolated chicken heart, which almost exclusively was released from the postganglionic neurons: (+)-tubocurarine (3×10−4 M) reduced the output to 12±6% (n=7) of the control. Stimulation of the two nerve trunks was equally effective in releasing ACh.-Evidence that a large number of postganglionic neurons receives bilateral innervation was based on two experimental series. (1.) The sum of the ACh outputs evoked by unilateral (separate) nerve stimulation of the right and the left vagus was higher than the bilaterally evoked output (100%) and increased with increasing frequencies (10, 20 and 40 Hz) from 115±13% to 131±9% (n=13). In the presence of 10−4 M 4-aminopyridine, unilaterally evoked output (40 Hz) was further increased from 131 to 176±5% (n=21).-(2.) In the presence of 4-aminopyridine plus hemicholinium-3 (2×10−5 M), unilateral nerve stimulation at 40 Hz evoked an output of ACh that decreased from 477 to 79 pmol g−1min−1 during a 20 min-period of stimulation due to transmitter depletion. Thereafter output of ACh evoked by stimulation of the contralateral nerve was reduced by 73% as compared to the control value (475 pmol g−1min−1; output without the preceding 20 min-stimulation).-It is concluded that a large number of parasympathetic postganglionic neurons of the chicken heart receives a dual excitatory input from both right and left vagus nerve.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01243281
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  • 2
    Electronic Resource
    Electronic Resource
    Acetylcholine overflow from isolated perfused hearts of various species in the absence of cholinesterase inhibition (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 296 (1977), S. 149-152 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine overflow ; Acetylcholine synthesis ; Parasympathetic nervous system ; Cholinesterase ; Physostigmine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The content of acetylcholine in the tissue and effluent of isolated hearts of various birds and mammals was determined in the absence of inhibition of cholinesterase. 2. Stimulation of both vagus nerves for 15 min at 20 Hz caused marked negative chronotropic effects in all species. Spontaneous or stimulation-induced overflow of acetylcholine into the effluents was not detected in mammals. In the avian heart, the order of spontaneous overflow was: duck = chicken 〉 pigeon, whereas the order of evoked overflow was: chicken 〉 pigeon 〉 duck. The acetylcholine overflow from the cat heart was below the limit of estimation (3 pmol g−1 min−1). In the chicken heart, the evoked overflow per min (284 pmol) was at least 95 times the overflow from the cat heart. 3. The average content of acetylcholine in the avian hearts was of the same order of magnitude (8.3–11.5 nmol/g) while the overflows ranged from 97 to 1615 pmol g−1 15 min−1. The acetylcholine content of cat and guinea-pig hearts was similar to that of avian hearts. 4. It is concluded that neither the spontaneous nor the stimulation-induced overflows of acetylcholine were correlated with the acetylcholine content in the tissue. The stimulation-induced overflow of acetylcholine into the effluent is much higher in avian than in mammalian hearts which, presumably, is due to differences in the amount of acetylcholine released from the terminal nerves.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508467
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of coronary perfusion rate on the hydrolysis of exogenous and endogenous acetylcholine in the isolated heart (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 296 (1977), S. 143-148 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine ; Cholinesterase ; Transmitter inactivation ; Coronary flow ; Isolated heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effect of perfusion rate on the hydrolysis of acetylcholine in isolated chicken hearts was studied by measuring both the spontaneous and the evoked output of endogenous acetylcholine into the perfusate in response to vagal stimulation and the arterio-venous difference of exogenous acetylcholine. 2. A decrease in the perfusion rate from 30 to 20 and 10 ml/min caused a graded and significant decline of both the spontaneous overflow of acetylcholine and the overflow evoked by stimulation of both vagus nerves (20 Hz, 1 ms, 40V) for 20 min. The spontaneous and evoked overflow at 30 ml/min were 2 and 3 times, respectively, the overflow at 10 ml/min. 3. Physostigmine (10−6M) raised both the spontaneous and the evoked acetylcholine outputs into the perfusate. The rise of the evoked output was much more pronounced at 10 ml/min (7.5-fold) than at 30 ml/min (2.5-fold) so that the differences in the output at these perfusion rates were abolished after inhibition of cholinesterase. 4. Although vagal stimulation in the presence of physostigmine caused an output of acetylcholine into the perfusate equivalent to the content of the heart determined before stimulation, no change of the cardiac acetylcholine content was observed. Thus the total acetylcholine content must have been resynthesized during the 20-min period of vagal stimulation. Physostigmine raised the acetylcholine content by the same extent, both before and after stimulation. 5. The arterio-venous difference of acetylcholine during infusion of this compound (10−7 M) for 10 min was increased from 37±8 to 56±7% (n=10) of the arterial concentration, when the perfusion rate was decreased from 30 to 10 ml/min. Physostigmine abolished the effect of the perfusion rate upon the appearance of acetylcholine in the effluent. Moreover, the arterio-venous differences were less than 5% after inhibition of cholinesterase. 6. It is concluded that extracellular inactivation of the parasympathetic transmitter of the heart is dependent on both the cholinesterase activity and the rate of the coronary flow.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508466
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  • 4
    Electronic Resource
    Electronic Resource
    DMPP and the adrenergic nerve terminal: Mechanisms of noradrenaline release from vesicular and extravesicular compartments (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 300 (1977), S. 131-138 
    Details
    ISSN: 1432-1912
    Keywords: DMPP ; Efflux of noradrenaline ; Release of noradrenaline ; Uptake of noradrenaline ; Neuronal noradrenaline compartments
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary DMPP (1,1-dimethyl-4-phenylpiperazine) in various concentrations between 1.6×10−6 M and 6.2×10−5 M was infused into isolated rabbit hearts to study the neuronal release and uptake of noradrenaline. 1. In the untreated heart, 2.2×10−5 M or 6.2×10−5 M DMPP caused an overflow of noradrenaline (22 or 300 ng/g, respectively) that was Ca2+-dependent. During infusion of 1.6×10−5 M DMPP, however, a Ca2+-independent overflow of noradrenaline was detected which was about 3.5-fold higher than the resting overflow (0.22 ng g−1 min−1) of noradrenaline and was maintained over the 21-min period of infusion of DMPP; the rate of contraction (155 beats/min) was also markedly elevated by maximally 60 beats/min. 2. The isolated heart removed about 50% of infused noradrenaline (3×10−8 M) from the perfusion fluid. The removal, which reflects neuronal netuptake, was reversibly reduced to about 5% during exposure to 1.6×10−5 M DMPP; half-maximal inhibition was caused by 3×10−6 M DMPP. 3. After pretreatment with reserpine and pargyline, the heart was perfused for 30 min with 1.2×10−6 M (−)noradrenaline (3H-labelled or unlabelled) and then washed with an amine-free solution. DMPP was infused beginning at 20 or 30 min after the start of the wash-out period, i.e. at a time when the efflux of noradrenaline originated from the adrenergic neurone. DMPP in concentrations of 1.6×10−5 M and 6.2×10−5 M caused an about 10-fold increase of the rate of efflux which was not altered by Ca2+-deprivation or by 10−5 M hexamethonium. Half-maximal facilitation was observed using 3.5×10−6 M DMPP. The facilitated efflux reached a maximum after 3 min and then declined gradually. The decline consists of 3 components with half-times of 3, 7 and 65 min. 4. It is concluded that various non-nicotinic effects of DMPP on the adrenergic neurone were separated from the well-known nicotinic release of noradrenaline by using low concentrations (〈2×10−5 M). The non-nicotinic increase in heart rate and in transmitter overflow evoked by DMPP presumably was due to (1) inhibition of re-uptake of spontaneously released noradrenaline and (2) to displacement of vesicular noradrenaline. Furthermore, the drug increased the release of noradrenaline from extravesicular stores (present after inhibition of monoaminoxidase), presumably by acceleration of the transmembranal efflux and by displacement of noradrenaline from extravesicular binding sites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505043
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  • 5
    Electronic Resource
    Electronic Resource
    The role of choline in the release of acetylcholine in isolated hearts (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 301 (1978), S. 207-215 
    Details
    ISSN: 1432-1912
    Keywords: Release of acetylcholine ; Choline ; Physostigmine ; Isolated heart ; Parasympathetic ganglionic transmission
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The concentrations of acetylcholine, choline and noradrenaline were estimated in the perfusate (overflow) of isolated hearts of chickens, cats, rabbits and guinea pigs. Neurotransmitter release was evoked by stimulation of both vagus nerves and by direct stimulation of the heart (field stimulation). 2. In the absence of exogenous choline and physostigmine, field stimulation at 20 Hz for 20 min caused an overflow of acetylcholine from the hearts of the 4 species investigated. During vagal stimulation, however, acetylcholine was detected only in the perfusate of the chicken heart. 3. Field stimulation for 2 min caused an overflow of 193 pmol g−1 min−1 acetylcholine and of 666 pmol g−1 min−1 noradrenaline from the guinea pig heart; pretreatment of the animals with reserpine blocked the release of noradrenaline but left the overflow of acetylcholine unaltered. 4. When the overflow of acetylcholine was evoked by vagal stimulation, infusion of 10−5 M choline into the cat and chicken heart caused an increase in the overflow that was 2–3-fold in the chicken heart and at least 23-fold in the cat heart (23 times the limit of estimation). In the presence of choline, the overflow of acetylcholine from the hearts of the 4 species evoked by field stimulation was 2–3 times the overflow in the absence of the drug. 5. Inhibition of the cholinesterase activity by 10−6 M physostigmine raised the overflow of acetylcholine evoked by vagal and/or by field stimulation uniformly by a factor of 2 to 3 in the 4 species investigated. In the cat heart, the combination of 10−5 M choline and 10−6 M physostigmine increased the overflow evoked by field stimulation for 20 min from 0.54 to 3.6 nmol g−1 20 min−1, i.e. by a factor of 7. 6. The cardiac content of acetylcholine was highest in the chicken heart (9.8 nmol/g) and lowest in the guinea pig heart (2.1 nmol/g). 7. The spontaneous efflux of choline from the isolated hearts after 15 min of perfusion ranged from 0.4 (cat) to 2.1 nmol g−1 min−1 (chicken) and was maintained at these levels for at least 1 h. 8. In the blood of chickens, cats and rabbits, the choline concentration was 0.5–1.0×10−5 M. 9. It is concluded that (1) an appreciable amount of acetylcholine released from parasympathetic nerves escapes into the circulation of isolated hearts, (2) the extent of the extracellular hydrolysis of acetylcholine is the same in avian and mammalian hearts, (3) the release of acetylcholine evoked by vagal stimulation is much smaller in the isolated cat heart than that in the chicken heart, because of an insufficient ganglionic transmission due to a deficiency in extracellular choline and finally (4) the amount of acetylcholine released by vagal stimulation is dependent on both the efflux of choline from extraneuronal sources and the overall density of the cholinergic innervation of the heart.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00507039
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  • 6
    Electronic Resource
    Electronic Resource
    Presence of muscarinic inhibitory and absence of nicotinic excitatory receptors at the terminal sympathetic nerves of chicken hearts (1976)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 295 (1976), S. 225-229 
    Details
    ISSN: 1432-1912
    Keywords: Sympathetic transmitter ; Nicotinic drugs ; Muscarinic drugs ; DMPP ; Isolated chicken heart ; Prejunctional receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nicotine (2×10−4 M) or acetylcholine (5.5×10−4 M) in the presence of 3×10−6 M atropine did not increase the rate or amplitude of contraction in isolated atria or ventricular strips of the chicken heart; both drugs also did not cause an output of noradrenaline or adrenaline and did not evoke antidromic discharges in the right sympathetic nerves of isolated perfused chicken hearts. In contrast, “high K+-solutions” evoked an output of noradrenaline and adrenaline and caused a burst of antidromic discharges. Dimethylphenylpiperazine (DMPP; 3.1×10−4 M), by a tyramine-like action, elicited a small output of noradrenaline and increased rate and amplitude of contraction, but did not evoke antidromic discharges. The noradrenaline output caused by DMPP was not reduced by lowering the extracellular Ca2+ concentration from 1.8 to 0.1125 mM.-Acetylcholine (10−5 and 10−4 M) inhibited the noradrenaline and adrenaline outputs evoked by electrical stimulation of the right sympathetic nerves (3 Hz, 1 ms, 30 V); the inhibition was blocked by 3×10−6 M atropine. —It is concluded that the terminal parts of sympathetic nerves of the chicken heart posses muscarinic inhibitory receptors but lack nicotinic excitatory receptors. Thus prejunctional nicotinic receptors are not an integral part of the terminal sympathetic neurone otherwise they would be present at this neurone in all species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505090
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  • 7
    Electronic Resource
    Electronic Resource
    Acetylcholine overflow during infusion of a high potassium —Low sodium solution into the perfused chicken heart in the absence and presence of physostigmine (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 299 (1977), S. 17-21 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine ; Physostigmine ; K+-induced acetylcholine release ; Choline uptake ; Chicken heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effect of infusion of a modified Tyrode's solution (“high K+-low Na+ solution”) into the isolated chicken heart on the content of acetylcholine in the tissue and the overflow of acetylcholine were compared to those evoked by vagal stimulation. 2. The release of acetylcholine was measured over 15-min periods of either stimulation of the vagus nerves (40 V, 1 ms) at 20 Hz or of infusion of the high K+-low Na+ solution (108 mM K+, 44 mM Na+). 3. Both stimuli caused a maximum overflow of acetylcholine in the first few minutes whether or not 10−6 M physostigmine was present. The overflow was maintained during the vagal stimulation at a constant rate of at least 35% the initial rate, whereas the overflow evoked by the high K+-low Na+ solution ceased after 5 min. Under the latter conditions, the size of the acetylcholine store available for release (overflow in the presence of physostigmine) was 41% of the total store. 4. Physostigmine (10−6 M) caused a 2–3-fold increase of the overflow of acetylcholine evoked either by nerve stimulation or by infusion of the high K+-low Na+ solution. Reduction of [Ca2+]o from 1.8 to 0.2 mM strongly reduced the overflow caused by either kind of stimulation. 5. The sum of the overflow evoked by the high K+-low Na+ solution and the cardiac content of acetylcholine after the stimulation did not exceed the cardiac content before stimulation. 6. In conclusion, infusion of a high K+-low Na+ solution caused an overflow of acetylcholine in the absence and presence of physostigmine that was similar to that evoked by nerve stimulation with respect to Ca2+-dependency and hydrolysis of the released acetylcholine. The rate of synthesis of acetylcholine maintaining a steady state release was high during nerve stimulation, but was blocked during infusion of the high K+-low Na+ solution, presumably by block of the high affinity uptake of choline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508632
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  • 8
    Electronic Resource
    Electronic Resource
    Interstitial washout and hydrolysis of acetylcholine in the perfused heart (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 318 (1982), S. 295-300 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine ; Choline ; Perfused heart ; Cholinesterase ; Interstitial washout
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The efflux of acetylcholine, of radioactively labelled acetylcholine and choline, into the venous effluent of the perfused chicken heart was studied to determine the kinetics of both interstitial washout and hydrolysis of acetylcholine. Stimulation of both cervical vagus nerves (e.g., for 5 s at 40 Hz) caused a release of acetylcholine, which appeared partially unhydrolyzed in the venous effluent, and reduced force of contraction and heart rate. For comparison labelled acetylcholine or choline was infused for 5 s into the heart and again the venous efflux of either substance was determined. It was found that the kinetics of efflux of acetylcholine or choline from the interstitial space were of first order. The mean half times were 16.2 s (after infusion of acetylcholine) and 17.9 s (after nerve stimulation) for acetylcholine and 17.9 s (after infusion of choline) for choline. In the interstitial space, radioactivity (sum of [3H]-acetylcholine and [3H]-choline formed from [3H]-acetylcholine) released by nerve stimulation declined mono-exponentially with a rate constant of 0.069 s−1 and a half time of 10 s (due to washout), whereas the concentration of unhydrolyzed [3H]-acetylcholine decreased in a multi-exponential fashion due to both washout and hydrolysis. The interstitial concentration of [3H]-acetylcholine reached the 50% level after 2.5 s. In conclusion, the long persistence of unhydrolyzed acetylcholine in the interstitial space of the heart appears to be due to an apparently low rate of hydrolysis. This, in turn, is responsible for the importance of diffusion and washout of acetylcholine from the interstitial space as significant factors of synaptic removal of acetylcholine. Moreover, the results support the notion that the sustained interstitial concentration of acetylcholine determines the long duration of cardiac responses to vagal stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501168
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  • 9
    Electronic Resource
    Electronic Resource
    4-Aminopyridine antagonizes the inhibitory effect of pentobarbital on acetylcholine release in the heart (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 312 (1980), S. 7-13 
    Details
    ISSN: 1432-1912
    Keywords: ACh release ; 4-Aminopyridine ; Heart ; Pentobarbital ; Tetracaine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of pentobarbital on acetylcholine (ACh) release, force of contraction and nervous conduction were studied in isolated heart preparations and in cervical vagus nerves, respectively. 4-Aminopyridine and tetracaine were used as pharmacological tools to eludicate the mode of action of pentobarbital. 1. 4-Aminopyridine (10−4 M) markedly increased the overflow of ACh from the isolated chicken heart evoked by electrical stimulation (1–50 Hz, 1 ms, 40 V) of the cervical vagus nerves. This effect of 4-aminopyridine was highest at low frequencies of stimulation (+ 226% at 1 Hz) and declined with increasing frequencies to reach a minimum augmentation of 22% at 30 Hz. 2. Pentobarbital and tetracaine dose-dependently decreased the evoked overflow of ACh from the isolated chicken heart. Half-maximal inhibition was observed at concentrations (IC50) of 1.4×10−4 M and 4×10−6 M, respectively. Much higher concentrations of pentobarbital were required to inhibit the conduction in vagal B-fibres (IC50=3×10−3 M) whereas the IC50 values of tetracaine for both inhibitory effects were nearly identical. 3. 4-Aminopyridine (10−4 M) antagonized the inhibitory effect of PB on the evoked overflow of ACh and shifted the concentration-response curve to the right. The 4-aminopyridine/pentobarbital antagonism was equally pronounced whether the release of ACh was evoked by vagal stimulation (preganglionic) or by field stimulation (pre- and postganglionic). 4. The negative inotropic effect of vagal stimulation in isolated atria of cats and chickens was weakened by pentobarbital (1–5×10−4 M) and enhanced by 4-aminopyridine (10−4 M). Again, 4-aminopyridine (10−4 M) antagonized the effect of pentobarbital. 5. In contrast to the effects of pentobarbital, the inhibition of ACh overflow produced by tetracaine was not antagonized by 4-aminopyridine. 6. The results strongly support the previous suggestion (Lindmar et al., 1979) that the inhibition by pentobarbital of the evoked overflow of ACh from the postganglionic parasympathetic neurones of the heart is due to a reduction of the Ca2+ inward current into the nerve terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00502566
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  • 10
    Electronic Resource
    Electronic Resource
    The isolated perfused chicken heart as a tool for studying acetylcholine output in the absence of cholinesterase inhibition (1976)
    Springer
    Journal of neural transmission 38 (1976), S. 9-14 
    Details
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In chicken hearts, the acetylcholine (ACh) output in response to vagal stimulation was easily detectable by gas chromatography even in the absence of cholinesterase inhibition. Eserine 10−6 M markedly increased the ACh output. In contrast, the ACh output from the perfused rabbit heart was not measurable in the absence of cholinesterase inhibition. Both ACh concentration and cholinesterase activity were higher in the chicken heart than in the rabbit heart. In conclusion, the isolated perfused chicken heart is at present a unique tool for studying the output of the parasympathetic transmitter in the absence of cholinesterase inhibition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01254136
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