There has been considerable interest recently in the identity of the chemical transmitter released from sensory nerve endings to cause antidromic vasodilatation in the skin. Both substance P (Lembeck, 1953) and adenosine triphosphate (ATP: Holton & Holton, 1954) are active vasodilators and have been found in extracts of dorsal roots and there is some evidence in favour of each of them being regarded as the transmitter. However, there is no evidence that substance P is released when sensory nerves are stimulated and until now the evidence that ATP is released has not been conclusive.When rabbits' ears are perfused with Locke's solution, antidromic stimulation of the great auricular nerve results in a specific increase in the optical density at 260 m,u in samples of the venous effluent (Holton & Holton, 1953).The difference between the absorption spectra of samples collected during stimulating and during control periods is typical of that produced by substances containing purine and pyrimidine rings, including ATP and its break-down products. Other evidence (Holton & Holton, 1954) showed that vasodilatation due to antidromic stimulation in the rabbit's ear was similar in its time course to that caused by injection of ATP. It was therefore suggested that stimulation of the great auricular nerve liberated ATP, which played some part in causing the vasodilatation in the intact ear, and passed into the circulation to appear in the effluent from the perfused ear. Holton & Holton's observations did not identify the absorbing substance as ATP nor did they exclude the possibility that the substance came from the blood. In the present work these experiments have been extended using a specific method for assaying ATP.It has now been shown that ATP is liberated when the great auricular nerve is stimulated and that it does not come from the blood.

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The bilateral removal of the carotid bodies and consequent denervation of the carotid sinuses, as a treatment for asthma, provided the opportunity to study the physiological effects of these procedures in the human being. METHODSThe subjects were two hospital patients with long-established bronchial asthma. Their histories and clinical condition have been described elsewhere (Wood, Frankland & Eastcott, 1965 A box bag respirator (Donald & Christie, 1949) was used to administer gas mixtures for periods of up to 4 min each and to record tidal volume and respiratory frequency.The gas mixtures were saturated with water vapour at room temperature and had the following composition: room air, 100 % oxygen, 10 % oxygen in nitrogen, 3 % carbon dioxide in air and 6 % carbon dioxide in air. 10 % oxygen was usually administered twice on each occasion. On some occasions arterial oxygen saturation was recorded with an Atlas ear oximeter which was calibrated against samples of arterial blood analysed by manometric Van Slyke estimations and was accurate to within + 4 %. Arterial blood pressure and pulse rate were measured at frequent intervals by auscultation and palpation respectively or by a Sanborn pressure transducer and recorder through a needle in the brachial artery. The frequency response was accurate from 0.5 to 15 c/s. Passive changes in posture were produced by tilting the subject on an Eve rocker which had been modified to allow a vertical position. Valsalva mannsuvres were performed by the subject blowing against a mercury column. RESULTS Chemoreceptor responsesSubject A. Before operation subject A responded normally by hyperpnoea to breathing 10% oxygen, 3 % C02 and 6% CO2. There was no cyanosis.At operation, both carotid bodies were removed and the adventitia was peeled off for about 2 cm on each side of the carotid bifurcations (Wood et al. 1965). Recovery was uneventful. Two weeks after operation the

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