Neurokinin A, eledoisin and substance P contracted strips of rabbit main pulmonary artery in a concentration-dependent manner with neurokinin A and eledoisin being 300fold more potent than substance P. Substance P methyl ester was inactive. Neurokinin A and substance P relaxed precontracted vascular strips provided that the endothelium was intact. The rank order of potency of the various agonists suggested the existence of a muscular SP-E type and possibly an endothelial SP-P type tachykinin receptor for the rabbit main pulmonary artery. Porcine coronary artery was devoid of excitatory muscular tachykinin receptors but contained an endothelial SP-P type receptor which, similar to that in the rabbit main pulmonary artery, mediated vasorelaxation. Stimulation of the muscular tachykinin receptor in the rabbit main pulmonary artery resulted in depolarization of the membrane of the smooth muscle cells. In the porcine coronary artery, activation of the endothelial tachykinin receptor produced hyperpolarization of the smooth muscle membrane in all probability through release of endothelium derived relaxing factor. Neurokinin A- and substance P-induced contractions of rabbit main pulmonary artery were not susceptible to inhibition by calcium antagonists and were not affected by pertussis toxin-induced inactivation of a guanine nucleotide binding regulatory protein (N.). It is, therefore, suggested that activation of the smooth muscle tachykinin receptor leads predominantly to a release of calcium from the sarcoplasmic reticulum and that N. is not involved in signal transductioft between the tachykinin receptor and the subsequent steps initiating contraction.
Weitere Kapitel dieses Buchs durch Wischen aufrufen
- Electrical and Mechanical Responses of Vascular Muscle to Tachykinins
J.-E. de Peyer
- Springer New York
Fallstudie Überschwemmungskarten/© Thaut Images | Fotolia