In the salivary reflex, not only secretory cells are activated, but also myo-epithelial cells are contracted to support these cells and promote the flow of saliva, and blood vessels dilate to meet the increased demands of the tissues. The various effector cells often receive nerves from both parts of the autonomic system, and interactions may occur when the nerves act on the same type of effector, or on different types of effectors. While in an experiment electrical stimulation of the sympathetic trunk may decrease a parasympathetic salivary flow by causing marked vasoconstriction, this does not occur in the salivary reflex, since the vasoconstrictors do not take part. On the contrary, the normal sympathetic vasoconstrictor tone of the resting gland is easily overcome by activity in parasympathetic vasodilator nerves when secretion starts. Pronounced synergism can be demonstrated between sympathetic and parasympathetic secretory nerves. In dogs, for instance, in which sympathetic secretion is beta-adrenoceptor-mediated, this is marked in the case of fluid secretion. In rats and rabbits, in which beta-receptors elicit secretion of amylase, the potentiating interaction among the nerves is striking when amylase secretion is considered. Even the random release of acetylcholine from the post-ganglionic parasympathetic axons, by itself insufficient to evoke secretion, can increase the sympathetic effects. Motor nerves interact with secretory nerves by causing myo-epithelial contraction, mechanically promoting secretion. Interactions between the nerves in their long-term regulatory function on the sensitivity of the acinar secretory and myo-epithelial cells can also be demonstrated.

It is generally assumed that the reaction of the human skin to the sting of the common nettle (Urtica Urens) is brought about by an unknown poison, present in the fluid of the nettle hair, which has the property of releasing histamine (or H-substance) from the epithelial cells. The nettle hair consists of a fine capillary tube calcified at its lower and silicified at its upper end and closed at the tip in the form of a little bulb. This bulb breaks off in a predetermined line when it comes in contact with the skin, leaving exposed a fine needle-like point formed by the upper tapering part of the hair. As a result of the pressure of contact this fine tube penetrates the skin and the compression of the bladderlike base injects the contained fluid into the minute wound. According to Haberlandt (1886) the active poison could be an enzyme, and the mechanism of the nettle sting would then be comparable with that of the bee sting, bee venom being a lecithinase which acts on lecithin forming a lytic substance (lysolecithin) which then in its turn releases histamine (Feldberg & Kellaway, 1937a, b). Haberlandt certainly excluded the possibility that formic acid is the active substance in nettle hairs, but he performed no experiments on the action of nettle hair extracts on isolated tissue preparations.Our experiments were started on the assumption that the pharmacologically active substance in the nettle hair acts by the release of histamine from the human skin. This might occur if the substance behaved like an antigen in the antigen-antibody reaction, or if it were an enzyme. However, a different and in some ways simpler explanation was found. The hair fluid itself contains histamine and in a high concentration. It was also found to contain acetylcholine in an even higher concentration and a third smooth muscle-contracting substance which has not yet been identified. The mechanism of the nettle sting reaction can be explained wholly, or at least in its main features, by the presence of histamine and acetylcholine in the hair fluid; there is no necessity to assume that the 'nettle poison' acts by releasing additional histamine from the human skin. It was further shown that histamine as well as acetylcholine occur not only in the hair fluid but also in the tissue of the leaves.

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SUMMARY1. The pressures in the ducts of the submaxillary, parotid and sublingual glands were recorded in cats under chloralose anaesthesia. A single stimulus applied to the parasympathetic glandular nerve caused a pressure rise, the size of which increased with the initial pressure. This response was abolished by a small dose of atropine.2. The effect was not due to salivary secretion, since the single stimulus caused salivation only exceptionally. Repetitive stimulation at frequencies too low to evoke secretion could produce summated pressure responses.3. The single stimulus applied to the chorda tympani was found to cause vasodilatation in the submaxillary gland. This was abolished by a small dose of atropine, together with the pressure rise in the duct. However, repetitive stimulation still caused marked vasodilatation but no pressure response. It was therefore inferred that the pressure rise obtained before atropine was not due to vasodilatation in the gland.4. It is concluded that the myoepithelial cells of the salivary glands are supplied with a parasympathetic motor innervation which can cause them to contract.5. Sympathetic stimulation caused no pressure rise when a single stimulus was given but only when repetitive stimulation was used at a frequency approaching that required for secretion.

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