Abstract
To clarify the effect of extracellular magnesium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2+ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10-8-10-5 M norepinephrine, were significantly potentiated at low Mg2+ (0.8 mM v. the normal, 1.2mM). High (1.6 and 2.0 mM) Mg2+ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC50 values for norepinephrine were found. The endothelium-dependent relaxations induced by 10-8-10-5 M acetylcholine were inhibited by high (1.6 and 2.0 mM) Mg2+. Lowering of the Mg2+ concentration to 0.8 mM or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC50 values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg2+ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg2+ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg2+ deficiency in the development of the cerebral vasospasm.
Original language | English |
---|---|
Pages (from-to) | 161-164 |
Number of pages | 4 |
Journal | Journal of Cerebral Blood Flow and Metabolism |
Volume | 11 |
Issue number | 1 |
State | Published - 1991 |
Externally published | Yes |
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Keywords
- Acetylcholine
- Cerebrovascular smooth muscle
- Contraction
- Endothelium-dependent relaxation
- Extra-cellular magnesium
- Norepinephrine
ASJC Scopus subject areas
- Endocrinology
- Endocrinology, Diabetes and Metabolism
- Neuroscience(all)
Cite this
Contractile and endothelium-dependent dilatory responses of cerebral arteries at various extracellular magnesium concentrations. / Faragó, Mária; Szabo, Csaba; Dóra, Eörs; Horváth, Ildikó; Kovách, Arisztid G B.
In: Journal of Cerebral Blood Flow and Metabolism, Vol. 11, No. 1, 1991, p. 161-164.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Contractile and endothelium-dependent dilatory responses of cerebral arteries at various extracellular magnesium concentrations
AU - Faragó, Mária
AU - Szabo, Csaba
AU - Dóra, Eörs
AU - Horváth, Ildikó
AU - Kovách, Arisztid G B
PY - 1991
Y1 - 1991
N2 - To clarify the effect of extracellular magnesium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2+ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10-8-10-5 M norepinephrine, were significantly potentiated at low Mg2+ (0.8 mM v. the normal, 1.2mM). High (1.6 and 2.0 mM) Mg2+ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC50 values for norepinephrine were found. The endothelium-dependent relaxations induced by 10-8-10-5 M acetylcholine were inhibited by high (1.6 and 2.0 mM) Mg2+. Lowering of the Mg2+ concentration to 0.8 mM or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC50 values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg2+ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg2+ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg2+ deficiency in the development of the cerebral vasospasm.
AB - To clarify the effect of extracellular magnesium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2+ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10-8-10-5 M norepinephrine, were significantly potentiated at low Mg2+ (0.8 mM v. the normal, 1.2mM). High (1.6 and 2.0 mM) Mg2+ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC50 values for norepinephrine were found. The endothelium-dependent relaxations induced by 10-8-10-5 M acetylcholine were inhibited by high (1.6 and 2.0 mM) Mg2+. Lowering of the Mg2+ concentration to 0.8 mM or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC50 values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg2+ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg2+ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg2+ deficiency in the development of the cerebral vasospasm.
KW - Acetylcholine
KW - Cerebrovascular smooth muscle
KW - Contraction
KW - Endothelium-dependent relaxation
KW - Extra-cellular magnesium
KW - Norepinephrine
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UR - http://www.scopus.com/inward/citedby.url?scp=0026098578&partnerID=8YFLogxK
M3 - Article
C2 - 1984000
AN - SCOPUS:0026098578
VL - 11
SP - 161
EP - 164
JO - Journal of Cerebral Blood Flow and Metabolism
JF - Journal of Cerebral Blood Flow and Metabolism
SN - 0271-678X
IS - 1
ER -