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1. Stimulation of left atrial receptors by distending balloons located at the junction between the pulmonary veins and the left atrium and in the body of the left atrium resulted in a diuresis in anaesthetized dogs.2. In the same dogs the diuresis was not consistently associated with a reduction in the antidiuretic activity of plasma as compared with that during the initial control period. The antidiuretic activity of dog plasma was assayed in water-loaded rats anaesthetized with ethanol.3. Intravenous injections of vasopressin suppressed a water diuresis in water-loaded dogs anaesthetized with chloralose. The changes in antidiuretic activity of dog plasma which resulted from these injections were reliably detected by the bio-assay in the rat.4. It is concluded that the diuretic response to the stimulation of left atrial receptors is not accompanied by a reduction in the plasma antidiuretic hormone level.

1 McN-A-343 (4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride) in concentrations of 10(-5) and 10(-4)M inhibits the stimulation-induced efflux of radioactivity from segments of rabbit ear artery that have previously been incubated with (-)-[(3)H]-noradrenaline, and also decreases the contractile response.2 The inhibitory effects of McN-A-343 (10(-5)M) on the efflux of radioactivity and the contractions induced by low frequencies of stimulation (2 and 5 Hz) are reversed by atropine, but atropine does not modify these effects with high frequencies of stimulation (20 and 50 Hz).3 McN-A-343 (10(-4)M) enhances the stimulation-induced efflux of radioactivity from guinea-pig atria that have previously been incubated with (-)-[(3)H]-noradrenaline, and prolongs the positive inotropic response. These effects are not modified by atropine.4 It is concluded that McN-A-343 has different effects on adrenergic transmitter release in the two tissues. In the artery, it acts as an agonist on muscarinic receptors of adrenergic terminals to inhibit transmitter release at low frequencies of stimulation. In the atria it enhances transmitter efflux from the tissue, largely by inhibiting re-uptake.

1. Fluorescence histochemical and pharmacological studies were made of the noradrenergic innervation of inferior venae cavae and left atria from 2- and 6-week-old chicks before, and following, treatment with 6-hydroxydopamine.2. Noradrenergic nerves in the younger animals appeared to be relatively resistant to the toxic effects of 6-hydroxydopamine.3. In the older animals, the time course of recovery from the effects of 6-hydroxydopamine appeared to reflect the rate of regeneration of destroyed noradrenergic nerves.4. Marked presynaptic supersensitivity to adrenaline and noradrenaline was observed in left atria and inferior venae cavae following treatment with 6-hydroxydopamine.

1. A reflex increase in heart rate in response to pulmonary vein distension was observed in decerebrate dogs. This increase could not be totally abolished by treatment with both propranolol and bretylium tosylate. Only bilateral cervical vagotomy abolished the reflex increase in heart rate.2. A significant increase in heart rate occurred in a total of seventeen spinal dogs during pulmonary vein distension.3. In seven spinal animals in which blood pressure was maintained by the continuous infusion of noradrenaline, the increase in heart rate could be totally prevented by cervical vagotomy.4. The time course of the increase in heart rate observed in the spinal animals was rapid, reaching maximum expression within 10 sec of pulmonary vein distension. Such a time course is dissimilar from that associated with pulmonary vein distension in intact or decerebrate dogs in which maximum increases in heart rate take 1-3 min to develop.5. It is concluded that the reflex tachycardia resulting from pulmonary vein distension may be mediated by both an efferent sympathetic and an efferent vagal pathway, the relative significance of each component being dependent upon the prevailing autonomic drive existent in the animal at any specific time.

1. The differences in spike discharge from atrial mechanoreceptors in vivo suggest the existence of different receptor types. To test this possibility, and to see how atrial receptors compare with other mechanoreceptors, their response was studied under comparable stimulus conditions.2. Sinusoidal length changes, with frequencies from 1 to 10 Hz and amplitudes of 1.5-5.0 mm at a given static extension, were imposed in situ on strips of atrial receptor areas of cats.3. The receptor response was evaluated from functional single fibres in terms of number of spikes per stimulus period, average discharge rate, instantaneous spike frequency, and phase angle between forcing function and instantaneous frequency.4. Irrespective of the fibre type, atrial fibres appear to originate from identical mechanoreceptors which sense length at low stimulus frequency and low stimulus amplitudes, but also sense velocity in the high frequency range and with large stimulus amplitudes.5. The difference in the discharge pattern and in the functional behaviour of the atrial fibres in vivo can be explained on the basis of identical receptors.6. The difference in the temporal occurrence of the atrial burst is still open to debate, but probably is related to the site of the receptor.

1. Single unit recordings from type B atrial receptors were obtained from slips of the left cervical vagus nerve during acute increases and decreases in atrial pressure produced by infusion of isotonic saline and withdrawal of blood.2. Atrial receptor discharge reached a peak frequency at the peak of the ;v' wave of the atrial pulse, a time when the rate of change of atrial pressure was zero.3. The receptor discharge exhibited hysteresis when increases in atrial pressure were compared to decreases in atrial pressure during circulatory volume expansion and haemorrhage, respectively. This hysteresis was not due to a change in atrial compliance.4. The hysteresis was still observed when the pulse pressure of the ;v' wave was plotted against receptor discharge.5. Type B atrial receptors did not show adaptation after 15 min of a sustained increase in left atrial pressure.6. Acute depression of atrial contractility with propranolol increased resting fibre discharge as a result of the associated increase in atrial pressure.

1. We recorded the electrical activity of single afferent cardiac fibres isolated from the third and fourth left thoracic sympathetic rami communicantes of anaesthetized cats. Their conduction velocities ranged from 12 to 32 m/sec.2. The endings of each fibre were localized to one cardiac chamber by mechanical probing of the opened heart performed at the end of the experiment.3. The impulse activity was spontaneous and, in fibres with atrial or ventricular endings, it was in phase with a particular atrial or ventricular event.4. This nervous activity increased during increases in pressure occurring in the chamber where the endings were located. Conversely, decreases in pressure were accompanied by decreased nervous discharge.5. In some experiments the left coronary artery was perfused at different flows and pressures. Brief decreases or increases in coronary flow and pressure decreased or increased, respectively, the discharge of fibres with atrial or ventricular endings. Fibres were excited by intracoronary injections of veratridine.6. Cessation of coronary pump flow increased the discharge of fibres with atrial or ventricular endings only when myocardial ischaemia was accompanied by signs of heart failure.7. These afferent cardiac sympathetic fibres which provide the spinal cord with continuous specific information on cardiac events are likely to contribute to the neural control of circulation.

1. Action potentials were recorded from fibres in the right cervical vagus, the receptor endings of which were localized to the endocardial surface of the superior vena caval-right atrial junction.2. Stretching the junction between the superior vena cava and the right atrium without obstructing venous return caused an increase in the discharge of these fibres. This increase in impulse frequency was similar to that caused by small changes in mean right atrial pressure (range 0-13.5 cm H(2)O).3. This evidence supports the earlier suggestion that stimulation of the right atrial receptors by stretching the superior vena caval-right atrial junction causes a reflex increase in heart rate.

1. Distension of the atrial appendages resulted in a diuresis, an increase in the rate of Na(+) excretion and an increase in heart rate.2. Both the urinary and heart rate responses to distension of the appendages were either abolished or much reduced by crushing the bases of the appendages.3. The diuresis in response to distension of the atrial appendages is similar to that previously described in response to distension of the pulmonary vein-atrial junctions by Ledsome & Linden (1968).4. It is concluded that stimulation of nerve endings within the atrial appendages results in a reflex increase in urine flow and heart rate.