Evidence for noradrenaline and adrenaline as sympathetic transmitters in the chicken.

1 The concentrations of noradrenaline and adrenaline in various organs, arterial plasma and venous outflow from isolated hearts of adult chickens have been determined. 2 The relative adrenaline concentrations (percentage of the sum of noradrenaline and adrenaline) in the heart (33%), spleen (16%) and brain (26%) were higher than those found in mammalian organs. Chemical sympathectomy by pretreatment with 6-hydroxydopamine caused a decrease of the noradrenaline and adrenaline concentrations in the heart to 20 and 23% and in the spleen to 16 and 29%, respectively. 3 Stimulation of the right sympathetic nerves, infusion of tyramine or infusion of a modified Tyrode solution containing 108mM K+ …

Inhibition by parasympathetic nerve stimulation of the release of the adrenergic transmitter

Isolated rabbit atria were perfused with Tyrode solution containing (+)-amphetamine. Electrical stimulation of the right postganglionic sympathetic fibres caused an output of noradrenaline which was significantly decreased by simultaneous stimulation of the vagus nerves.

Short- and long-term effects of vinblastine on the rat adrenal medulla

The effects of a single high dose (10mg/kg) of vinblastine (vb) sulfate (“Velbe”, Lilly) on the ultrastructure, catecholamine (CA) content and activity of CA-synthesizing enzymes of the rat adrenal medulla were studied for up to 120h after intravenous injection of the drug.

Unterschiede zwischen Tyramin und Dimethylphenylpiperazin in der Ca++-Abhängigkeit und im zeitlichen Verlauf der Noradrenalin-Freisetzung am isolierten Kaninchenherzen

On the perfused rabbit heart a constant infusion of tyramine released noradrenaline continuously and independently of the external Ca++ concentration. In contrast, noradrenaline release by DMPP was only transient and required the presence of Ca++.

Über einen durch Nicotinreceptoren vermittelten Block an der postganglionären sympathischen Nervenfaser

Der Einflu� von Atropin auf die Noradrenalin-Freisetzung durch Acetylcholin

A muscarinic inhibition of the noradrenaline release evoked by postganglionic sympathetic nerve stimulation

1. The noradrenaline output from isolated rabbit hearts perfused with Tyrode solution was estimated fluorimetrically. The postganglionic sympathetic nerves of the heart were stimulated (10 shocks/sec; 1 msec) for three 1 min periods with intervals of 10 min. 2. The noradrenaline output evoked by 3 consecutive stimulation periods decreased exponentially. 3. Acetylcholine (10−9–10−6 g/ml) administered continuously one min before to one min after the second stimulation caused a dose-dependent reduction of the noradrenaline output evoked by the second stimulation to as low as 19% of the normal value. Acetylcholine in the concentrations applied did not cause a noradrenaline output by itself. 4. …

4-Aminopyridine (4AP) Enhances Acetylcholine Output from the Rat Cerebral Cortex in vivo

Publisher Summary This chapter discusses a study to analyze the effect of 4-aminopyridine (4AP) administration on cortical acetylcholine (ACh) output. The study was done on adult male Wistar rats under urethane or pentobarbital anesthesia. A small Perspex cylinder filled with eserinized Ringer solution was applied on the exposed cerebral cortex. The solution in the collecting cylinder was removed every 10 min and its ACh content was determined by bioassay on the dorsal muscle of the leech. In urethane anaesthetized rats, the control ACh output was 0.98 ± 0.16 ng/min/cm2 and the administration of 4AP (3 mg/kg i.p.) was followed by a rapid increase in ACh output lasting at least 40 min. The i…

The interferance of muscarinic receptors with the noradrenaline release from sympathetic nerve endings caused by nicotinic agents.

A muscarinic mechanism inhibiting the release of noradrenaline from peripheral adrenergic nerve fibres by nicotinic agents.

Subtypes of muscarinic receptor on cholinergic nerves and atrial cells of chicken and guinea-pig hearts

1. Electrically driven chicken and guinea-pig atria were used to investigate the negative inotropic effects of the muscarinic agonists methacholine and acetylcholine (ACh). The release of ACh from isolated hearts into the perfusate in response to (preganglionic) vagal or (pre- and postganglionic) field stimulation was bioassayed on the guinea-pig ileum or determined by labelling with [3H]-choline. 2. Concentration-response curves for the negative inotropic effect of methacholine were shifted to the right by pirenzepine in various concentrations (0.03 to 10 mumol l-1). The pA2 values were 7.76 in chicken atria and 6.53 in guinea-pig atria. Pirenzepine and atropine antagonized the negative in…

Autoinhibition of nicotinic release of noradrenaline from postganglionic sympathetic nerves

1. The effects of nicotine, DMPP (1,1-dimethylphenylpiperazine) and acetylcholine (plus atropine) on the isolated rabbit heart were investigated. Heart rate, amplitude of contraction, coronary flow and output of noradrenaline into the perfusate were recorded. Noradrenaline was estimated fluorimetrically. 2. All nicotinic drugs evoked a dose-dependent output of noradrenaline and increased the rate and the amplitude of contraction. Increases of heart rate in response to nicotine and DMPP and increases of amplitude of contraction in response to all nicotinic drugs were clearly related to the output of noradrenaline. 3. The dose-response curves of the noradrenaline output evoked by nicotine, DM…

Untersuchungen �ber die Noradrenalin-Freisetzung durch Acetylcholin am perfundierten Kaninchenherzen

Die Wirkung veranderter Elektrolyt-Konzentrationen auf die Nordrenalin-Abgabe durch Acetylcholin wurde am isolierten, perfundierten Kaninchenherzen untersucht. Acetylcholin wurde in einer Konzentration von 3 × 10−5 g/ml 30 sec lang in die Aortenkanule infundiert. Die Perfusionsflussigkeit enthielt Atropin (3 × 10−6 g/ml) wahrend der ganzen Versuchsdauer. Die von den Herzen in das Perfusat abgegebenen Catecholamine wurden fluorimetrisch bestimmt; auserdem wurden die Herzfrequenz, die Kontraktionsamplitude und der Coronardurchflus registriert.

Die Hemmung der Noradrenalin-Abgabe durch Acetylcholin am sympathisch gereizten, isolierten Kaninchenherzen / The Inhibitory Effect of Acetylcholine on the Release of Noradrenaline from Isolated Rabbit Hearts Stimulated Sympathetically

Nicotinartig wirkende Substanzen setzen aus chromaffinen Zellen und aus sympathischen Nervenendigungen Noradrenalin (NA) frei. Am isolierten Saugetierherzen wird diese NA-Freisetzung aber gehemmt, wenn gleichzeitig Muscarinreceptoren z. B. durch Acetylcholin (ACh) oder Methacholin erregt werden (Lindmau Loffelholz u. Muscholl

Storage and release of false transmitters after infusion of (+)- and (?)-?-methyldopamine

Rabbits were given an infusion of 10 mg/kg (−)- or 30 mg/kg (+)-α-methyldopamine and killed after 135 min. The noradrenaline content of the heart was decreased to 26±5 and 34±2%, respectively, of the control value. After infusion of the (+)-isomer the missing noradrenaline was replaced by (−)-α-methylnoradrenaline. Electrical stimulation of the sympathetic nerves or infusion of acetylcholine plus atropine caused an output of noradrenaline and (−)-α-methylnoradrenaline from the isolated heart. The two amines were released in the same proportion as they were stored in the heart and the total output of both amines equalled the output of noradrenaline from control hearts. Nerve stimulation caus…

Nicotinic drugs and postganglionic sympathetic transmission

1. Isolated rabbit hearts with the sympathetic nerves attached were perfused with Tyrode solution. The noradrenaline output into the perfusate was measured fluorimetrioally. 2. When the niootinic autoinhibition produced by infusions of nicotine, DMPP, or acetylcholine (in the presence of atropine) was fully developed, the output of noradrenaline evoked by electrical stimulation of the postganglionic sympathetic nerves was not depressed. 3. Acetylcholine in the presence of atropine produced a transitory facilitation of the noradrenaline output evoked by sympathetic nerve stimulation. 4. Prolonged infusion of DMPP caused an adrenergic neurone block which was not observed after nicotine, or ac…

Die Hemmung der Noradrenalin-Abgabe durch Acetylcholin am sympathisch gereizten, isolierten Kaninchenherzen

EFFECTS OF 4-AMINOPYRIDINE ON ACETYLCHOLINE OUTPUT FROM THE CEREBRAL CORTEX OF THE RAT in vivo

Abstract 1 The effects of 4-aminopyridine (4AP) on the output of acetylcholine (ACh) from the cerebral cortex were investigated in unanaesthetized freely moving rats and in anaesthetized rats by means of the `cup technique'. ACh was determined by bioassay on the dorsal muscle of the leech. 2 In unanaesthetized rats intraperitoneal injection of 4AP (3 mg/kg) had no effect on the cortical output of ACh. 3 After injection of morphine (10 mg/kg s.c.), which depressed the spontaneous output of ACh, 4AP increased the cortical output to a level significantly higher than that determined before morphine injection. 4 In rats anaesthetized with either urethane or pentobarbitone, drugs known to decreas…