血管周围应用血管加压素对猫脑软脑膜动脉的收缩作用。

Contractile effects of perivascularly applied vasopressin on the pial artery of the cat brain.

作者信息

Nakai M

机构信息

Department of Cardiovascular Dynamics, National Cardiovascular Centre Research Institute, Osaka, Japan.

出版信息

J Physiol. 1987 Jun;387:441-52. doi: 10.1113/jphysiol.1987.sp016583.

DOI:10.1113/jphysiol.1987.sp016583

PMID:3656181

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1192514/

Abstract

The effects of perivascularly applied vasopressin on the diameter of pial arteries (control 298 +/- 14 S.E. micron) of the brain were examined after chronic implantation of a cranial window in fifteen anaesthetized cats. 2. Application of vasopressin resulted in a dose-dependent contraction. The threshold concentration for contraction was 3 X 10(-10) M, the half-maximal effective concentration (ED50) (1.6 +/- 0.2) X 10(-9) M, and the maximum reduction in artery diameter 37 +/- 2%. 3. The contraction was powerfully inhibited by perivascular application of a 10(-7) M solution of the vasopressin antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin. 4. Perivascular application of noradrenaline induced a dose-dependent contraction of the pial artery. The ED50 was (8.9 +/- 2.5) X 10(-7) M, and the maximum reduction in artery diameter was 33 +/- 2%. 5. Such noradrenaline-induced contraction was not modified at all in the presence of a subthreshold dose (2 X 10(-10) M) of vasopressin (P greater than 0.05, for the over-all difference in size of the contraction, ED50 and maximum contraction). 6. In another experimental setting it was also found that neither the subthreshold nor a suprathreshold (10(-9) M) dose of vasopressin modified the contraction induced by 10(-6) M-noradrenaline (P greater than 0.05, compared to the contraction in the absence of vasopressin). 7. Thus a powerful and sensitive contractile response of the pial arteries to perivascularly applied vasopressin was demonstrated. However, the modifying effect of vasopressin on the contraction induced by perivascularly applied noradrenaline was minimal.

摘要

在15只麻醉猫慢性植入颅骨视窗后，研究了血管周围应用加压素对脑软膜动脉直径（对照为298±14标准误微米）的影响。2. 应用加压素导致剂量依赖性收缩。收缩的阈浓度为3×10⁻¹⁰ M，半数最大有效浓度（ED50）为（1.6±0.2）×10⁻⁹ M，动脉直径最大缩小37±2%。3. 血管周围应用10⁻⁷ M的加压素拮抗剂[1-(β-巯基-β,β-环戊亚甲基丙酸),2-(O-甲基)酪氨酸]精氨酸加压素可强烈抑制该收缩。4. 血管周围应用去甲肾上腺素可引起软膜动脉剂量依赖性收缩。ED50为（8.9±2.5）×10⁻⁷ M，动脉直径最大缩小33±2%。5. 在存在阈下剂量（2×10⁻¹⁰ M）加压素的情况下，这种去甲肾上腺素诱导的收缩完全没有改变（收缩大小、ED50和最大收缩的总体差异，P＞0.05）。6. 在另一个实验设置中还发现，阈下剂量（2×10⁻¹⁰ M）或阈上剂量（10⁻⁹ M）的加压素均未改变10⁻⁶ M去甲肾上腺素诱导的收缩（与不存在加压素时的收缩相比，P＞0.05）。7. 因此，证明了软膜动脉对血管周围应用加压素有强大而敏感的收缩反应。然而，加压素对血管周围应用去甲肾上腺素诱导的收缩的调节作用很小。