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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 ['H]-choline. (Pz) and atropine were 40 and 5.4 nmol -'in chicken atria and 330 and 3.5 nmol '-', respectively, in guineapig atria. Thus, the respective potency ratios (IC0pJIC5j,trope) were 7.4 and 94.3 in the two species.3 Pirenzepine in low concentrations increased the release of unlabelled and 'H-labelled ACh from isolated hearts evoked by vagal and field stimulation only in chicken, but not in guinea-pigs. The halfmaximally-effective concentration of pirenzepine was about 30 nmol I' in the chicken heart, whereas, in the guinea-pig heart, an increased release was observed at 300 nmol I-'. (+ )-Tubocurarine [(+ )-Tc; 100 pmol I-'] reduced the release of ACh evoked by (preganglionic)vagal stimulation to a (+ )-Tc-resistant release of about 30%. The time-course of the neuronal release of['H]-ACh was markedly altered: the onset was delayed and the termination was extended beyond the period of stimulation ( min or 5 s) by several seconds. The (+)-Tc-resistant release was nearly abolished by 30 nmol I' pirenzepine. 5 In conclusion, the pre-and post-synaptic muscarinic receptors of the parasympathetic neuroeffector junction of the heart both belong to the M,-subtype in the chicken and to an M2-subtype in the guinea-pig. Block of the nicotinic ganglionic transmission in the chicken heart by (+ )-Tc unmasked a muscarinic transmission, which presumably was mediated through M,-receptors stimulating a low and prolonged postganglionic release of ACh.

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In anesthetized rats, the choline levels of cerebrospinal fluid and plasma obtained from blood collected from peripheral vessels (carotid artery, cardiac vessels) and from the transverse sinus were determined with a radioenzymatic assay. Cortical release of choline was studied using the "cup technique." The plasma choline level of the peripheral blood (11.5 mumol/L) was lower than that of the sinus blood. The resulting cerebral arterio-venous difference of choline was negative (3.2 mumol/L) and reflected the net release of choline from the whole brain. The plasma choline levels were not different irrespective of whether the rats were anesthetized with ether, urethane, or pentobarbital. However, the choline level of the cerebrospinal fluid, which normally was lower than the plasma choline levels, was increased by urethane anesthesia to a level between the arterial and venous plasma concentrations of the brain. In old rats (24 months), the choline level of the cerebrospinal fluid was significantly lowered, when compared with the results obtained with younger rats (2-4 months). In rats kept on a low-choline diet for 2 weeks, the plasma choline level of the peripheral blood was reduced to 51% of the control. The effect on the choline level of the sinus blood was smaller; the cerebral arterio-venous difference of choline was not reduced (it was even slightly enhanced). Likewise, the choline level of the cerebrospinal fluid and the cortical release of choline were not altered. Intraperitoneal administration of oxotremorine in pentobarbital-anesthetized rats kept on a low-choline diet increased the plasma levels of choline.(ABSTRACT TRUNCATED AT 250 WORDS)

I 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 108 mM K+ and 44 mM Na+ caused an output of both noradrenaline and adrenaline into the perfusate of isolated hearts. The relative adrenaline concentration in the perfusate (20-28%) was not significantly different from the relative adrenaline concentration remaining in these hearts (19-22%). In the individual experiments, the noradrenaline: adrenaline ratios of the stimulation perfusates were positively correlated with the ratios found in the hearts. 4 The effects of noradrenaline and adrenaline on cardiac rate and tension development were studied in spontaneously beating right atria and electrically driven left atria, respectively. In addition, the arterial pressure rise in response to noradrenaline or adrenaline was measured in chickens. It was found that the cardio-vascular potency of noradrenaline, as reflected by the increases in heart rate, cardiac tension development and arterial blood pressure, was not significantly different from that of adrenaline. 5 It is concluded that, in the chicken heart and spleen, both noradrenaline and adrenaline act as sympathetic neurotransmitters.