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Substance P‐induced relaxation and hyperpolarization in human cerebral arteries
Author(s) -
Petersson Jesper,
Zygmunt Peter M.,
Brandt Lennart,
Högestätt Edward D.
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb15893.x
Subject(s) - hyperpolarization (physics) , cerebral arteries , vasodilation , medicine , nitric oxide , muscle relaxation , endothelium , population , relaxation (psychology) , anesthesia , artery , cardiology , chemistry , nuclear magnetic resonance spectroscopy , stereochemistry , environmental health
1 Vascular effects of substance P were studied in human isolated pial arteries removed from 14 patients undergoing cerebral cortical resection. 2 Substance P induced a concentration‐dependent relaxation in the presence of indomethacin. No relaxation was seen in arteries where the endothelium had been removed. 3 N ω –nitro‐L‐arginine (l‐NOARG, 0.3 mM) abolished the relaxation in arteries from six patients. The relaxation was only partially inhibited in the remaining eight patients, the reduction of the maximum relaxation being less than 50% in each patient. 4 The L‐NOARG‐resistant relaxation was abolished when the external K + concentration was raised above 30 mM. 5 Substance P caused a smooth muscle hyperpolarization (in the presence of L‐NOARG and indomethacin), but only when the artery showed an L‐NOARG‐resistant relaxation. 6 The results indicate that nitric oxide is an important mediator of endothelium‐dependent relaxation in human cerebral arteries. Furthermore, another endothelium‐dependent pathway, causing hyperpolarization and vasodilatation, was identified in arteries from more than half the population of patients.