小脑顶核
刺激
内分泌学
化学
内科学
硝基精氨酸
乙酰胆碱
一氧化氮
苯肾上腺素
网状结构
血管舒张
麻醉
一氧化氮合酶
医学
血压
出处
期刊:American Journal of Physiology-regulatory Integrative and Comparative Physiology
[American Physiological Society]
日期:1992-11-01
卷期号:263 (5): R1156-R1161
被引量:63
标识
DOI:10.1152/ajpregu.1992.263.5.r1156
摘要
The endothelium-derived relaxing factor, probably NO, is a potent vasodilator that mediates the vasodilating action of acetylcholine (ACh). We studied whether NO participates in the cholinergic cerebrovasodilation elicited by stimulation of the cerebellar fastigial nucleus (FN). Rats were anesthetized with halothane and ventilated. FN or pontine reticular formation (PRF) were stimulated through microelectrodes. Hypertension was prevented by spinal cord transection with arterial pressure maintained by intravenous phenylephrine. Cerebral blood flow (CBF) was continuously monitored through a cranial window over the sensory cortex by a laser-Doppler probe. The window was superfused with Ringer solution (pH 7.3-7.4; 37 degrees C). During Ringer superfusion FN stimulation (100 microA; 50 Hz) increased CBF by 90 +/- 7% (n = 27; P < 0.001, analysis of variance and Tukey's test) and PRF stimulation (100 microA; 100 Hz) by 128 +/- 18% (P < 0.001; n = 9). Superfusion with the guanylyl cyclase inhibitor methylene blue (MB) (1 mM) attenuated the CBF increase elicited by FN stimulation by 77 +/- 3% (n = 22; P < 0.001). MB did not affect the CBF increase elicited by PRF stimulation (+98 +/- 18%; n = 9; P > 0.05). Similarly, superfusion with the NO-synthase inhibitor nitro-L-arginine (L-NA) attenuated the CBF increase elicited by FN stimulation (-67 +/- 3%; n = 14; P < 0.001 from Ringer) but not PRF stimulation (P > 0.05; n = 9). The CBF increases elicited by FN stimulation were not affected by the inactive isomer of nitroarginine, D-NA (P > 0.05; n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)
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