SUlMMARY1. In anaesthetized cats tetanic contraction of the hind-limb muscles, elicited by stimulating the ventral roots L 6-S 1, caused a rise of arterial -blood pressure, usually accompanied by small increases in heart rate and pulmonary ventilation: in decerebrate cats, all components of the response were much increased.2. With tetani of different strengths, obtained by stimulating with different intensities at the same frequency, the pressor response increased with increasing tension.3. When muscle contraction had been abolished by gallamine, or when dorsal roots L 6-S I had been sectioned, ventral root stimulation no longer caused a pressor response. The response is therefore a reflex, initiated in the exercising limb.4. The pressor response was not affected by section of all articular nerves to knee and ankle joints, or by section of the vagi. The stimulus therefore originates in the contracting muscles alone.5. The pressor response is potentiated by occluding the circulation through the working muscles. Reasons are discussed for concluding that the stimulus is chemical rather than mechanical, and that the 'metabolic receptors' for this exercise reflex are the free endings of group III and IV sensory nerve fibres located around the blood vessels.

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The concept of vasodilator metabolites diffusing through the interstitial fluid to act directly on the vessel walls has never accounted adequately for the vasodilatation observed in a contracting muscle; for this dilatation is not confined to the capillaries and arterioles, but extends to the small intramuscular arteries and even to the larger arteries outside the muscle. In previous experiments, in which the vasodilatation was registered by the increase in venous outflow from the muscle, the post-contraction hyperaemia was thought to be produced in the main by an axon reflex in vasodilator nerve fibres, for it was grossly impaired by local anaesthetics, botulinum toxin or large, 'paralysing' doses of nicotine (Hilton, 1953(Hilton, , 1954. However, the nature of any nerve fibres involved remained obscure, since the post-contraction hyperaemia was not affected by chronic lumbar sympathectomy or posterior root ganglionectomy.It was shown over twenty years ago that the femoral artery itself dilates after contraction of the muscles of the lower leg, even when all the nerves to the limb are divided (Schretzenmayr, 1933;Fleisch, 1935). This reaction therefore had also been thought to be due to an axon reflex. It was abolished by local application to the artery, below the site of measurement, of phenol or cocaine, hence the responsible conducting elements appeared to run in the artery wall. Experiments now carried out on this dilator response of the femoral artery have confirmed these findings. Further, the femoral artery response has been found to be affected by drugs and surgical procedures in exactly the same way as the major part of the post-contraction hyperaemia. They both appear to be part of one and the same vascular reaction with a common conducting mechanism, and, since no known system of nerve fibres can be shown to be responsible, it is suggested that the conduction is effected by the smooth muscle of the artery wall.

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