[Vascular effects of neurokinins in humans]

Neurokinins (mainly substance P and neurokinin A) are released by sensitive nerve fibres. These fibres have been found in the vascular wall of arteries and veins of many vascular regions, particularly in nasal mucosa vessels, temporal and coronary arteries and saphenous veins. Substance P causes vascular relaxation by stimulating NK1 endothelial receptors. This relaxant effect is mediated, according to the vessels, by nitric oxide (NO), prostanoids or endothelium-dependent hyperpolarizing factor (EDHF). Capsaïcin, which induces the release of neurokinins, and neurokinin A can cause contractions of some vascular preparations, suggesting the existence of smooth muscle NK2 receptor associated with contraction. The vasodilatation induced by substance P injection appears reduced in patients with cardiovascular risk factors. The clinical development of specific neurokinin receptor antagonists may give the opportunity to specify the role of neurokinins in systemic vascular diseases. The results already obtained after repeated local applications of capsaïcin (to reduce local levels of neurokinins) in vasomotor rhinitis and urticaria suggest that the vascular effects of neurokinins may participate in the clinical expression of these diseases.