Substance P-induced relaxation and hyperpolarization in human cerebral arteries

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Substance P-induced relaxation and hyperpolarization in human cerebral arteries. / Petersson, Jesper; Zygmunt, Peter M; Brandt, Lennart; Högestätt, Edward D.

I: British Journal of Pharmacology, Vol. 115, Nr. 6, 07.1995, s. 889-94.

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T1 - Substance P-induced relaxation and hyperpolarization in human cerebral arteries

AU - Petersson, Jesper

AU - Zygmunt, Peter M

AU - Brandt, Lennart

AU - Högestätt, Edward D

PY - 1995/7

Y1 - 1995/7

N2 - 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 omega-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.

AB - 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 omega-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.

KW - Adult

KW - Aged

KW - Benzopyrans/pharmacology

KW - Cerebral Arteries/drug effects

KW - Cromakalim

KW - Dose-Response Relationship, Drug

KW - Endothelium, Vascular/drug effects

KW - Female

KW - Humans

KW - Male

KW - Membrane Potentials/drug effects

KW - Middle Aged

KW - Pyrroles/pharmacology

KW - Substance P/pharmacology

KW - Vasodilation/drug effects

KW - Vasodilator Agents/pharmacology

U2 - 10.1111/j.1476-5381.1995.tb15893.x

DO - 10.1111/j.1476-5381.1995.tb15893.x

M3 - Article

VL - 115

SP - 889

EP - 894

JO - British Journal of Pharmacology

T2 - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 1476-5381

IS - 6

ER -