ISSN:
1440-1681
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
1. The effects of NG-nitro-L-arginine (l-NNA; 20mg/kg bodyweight (BW), i.v.) and metyrapone (300 mg/kg BW, s.c.) on acetylcholine (ACh)-induced depressor responses were investigated in anaesthetized rats.2. Acetylcholine (0.05,0.5,5 μg/kg BW, i.v.) dose-dependently evoked a sharp fall in mean blood pressure (BP) followed by a slow recovery under control conditions.3. Basal BP level was elevated when rats were treated with l-NNA, indicating endogenous nitric oxide (NO) participated in BP regulation. However, pretreatment with l-NNA did not attenuate but rather augmented the ACh-induced maximum vasodilation. In contrast, the time for recovery of mean BP to the pre-ACh administration level was shortened by l-NNA. These observations suggested that ACh-induced vasodilation consisted of two phases: a sharp and transient fall (phase 1) that was resistant to l -NNA followed by a longer depressor response (phase 2) that was suppressed by l-NNA.4. To examine whether augmentation of phase 1 by l-NNA resulted from the elevation of basal BP, an appropriate dose of phenylephrine was infused to obtain similar BP elevation. Phenylephrine infusion augmented the phase 1 in a similar manner to l-NNA pretreatment but showed little effect on phase 2, supporting the selective inhibition of phase 2 by l-NNA.5. The s.c. pretreatment with metyrapone for 3 days failed to attenuate phase 1. Thus, the involvement of endothelium-derived hyperpolarizing factor that could be formed by a metyrapone-sensitive oxidase in phase 1 was unlikely.6. These results suggest that some factor(s), which is not inhibitable by l-NNA or metyrapone, may induce the phase 1 depressor response to ACh while NO is responsible for the phase 2 response. The mechanism inducing the phase 1 response remains to be identified.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1440-1681.1998.tb02244.x
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