Article date: July 1995
By: Jesper Petersson, Peter M. Zygmunt, Lennart Brandt, Edward D. Högestätt, in Volume 115, Issue 6, pages 889-894
Vascular effects of substance P were studied in human isolated pial arteries removed from 14 patients undergoing cerebral cortical resection.
Substance P induced a concentration‐dependent relaxation in the presence of indomethacin. No relaxation was seen in arteries where the endothelium had been removed.
Nω–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.
The L‐NOARG‐resistant relaxation was abolished when the external K+ concentration was raised above 30 mM.
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.
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.
Vascular effects of substance P were studied in human isolated pial arteries removed from 14 patients undergoing cerebral cortical resection.
Substance P induced a concentration‐dependent relaxation in the presence of indomethacin. No relaxation was seen in arteries where the endothelium had been removed.
Nω–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.
The L‐NOARG‐resistant relaxation was abolished when the external K+ concentration was raised above 30 mM.
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.
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.
DOI: 10.1111/j.1476-5381.1995.tb15893.x
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