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Kinins and the Peripheral and Central Nervous Systems

  • Chapter
Bradykinin, Kallidin and Kallikrein

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 25 / 1))

Abstract

In the previous edition of this section of the Handbook, the primary focus on kinins, with regard to their relationships with the nervous system, was on their ability to stimulate chemoreceptors for pain in animals and especially in man (Armstrong, 1970). Direct application of bradykinin to an exposed cantharidin blister area on the forearm of human subjects causes a slightly delayed, burning type of pain. This reaches maximum in about 1 min and gradually lessens if the kinin is not removed. An after-pain may occur when the kinin is washed from the area. Tachyphylaxis developes with repeated applications at short intervals to the blister area but not usually if pain is induced by administration of kinin by other routes such as by intraarterial (i.a.) injection. Bradykinin, kallidin, and substance P were the most potent algesic agents evaluated with the cantharidin blister area technique. Burning pain is also evoked in man by intradermal and i.a. injections of bradykinin; i.p. administration causes pain most often described as cramping or colicky (Lim et al., 1967), although the pain was associated with sensations of pressure, distention, or burning in some subjects. The algesic effect of kinins, other peptides and agents such as histamine, acetylcholine, and 5-hydroxytryptamine is thought to be due primarily to stimulation of chemoreceptors on free nerve endings located in the paravascular connective tissue spaces around capillaries and venules (Lim, 1968; Armstrong, 1970). Degeneration after dorsal root ganglionectomy of sensory nerves surrounding small blood vessels has been shown in animals to prevent elicitation of pain by i.a. injections of algesic agents to the denervated limb while sympathectomy, which did not alter the paravascular sensory nerves, had no effect on the response (Guzman et al., 1962; Lim, 1968). With few exceptions, when bradykinin is injected i.v., i.m., or s.c., it does not evoke pain (Kantor et al., 1967; Lim, 1970), apparently because of rapid inactivation before it reaches the appropriate receptors.

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  1. W. G. Clark
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    Ervin G. Erdös

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Clark, W.G. (1979). Kinins and the Peripheral and Central Nervous Systems. In: Erdös, E.G. (eds) Bradykinin, Kallidin and Kallikrein. Handbook of Experimental Pharmacology, vol 25 / 1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67301-6_9

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