Abstract
Plasma creatine phosphokinase, lactic dehydrogenase, glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase activities significantly increased in rats immersed in 23°C water for 6 hr after restraint (water immersion stress). The stress-induced rises in the four enzymes were significantly prevented by the intraperitoneal injection of 6-hydroxydopamine (80 mg/kg), propranolol (1 and 10 mg/kg) or timolol (1 and 10 mg/kg) but not by phentolamine (0.1–10 mg/kg) and atropine (0.1–10 mg/kg). The stress also significantly increased plasma urea nitrogen and glucose levels; however, neither propranolol (0.1–10 mg/kg) nor timolol (0.1–10 mg/kg) did affect these levels. On the other hand, 6-hydroxydopamine (80 mg/kg) and phentolamine (10 mg/kg) slightly but significantly prevented the increase in plasma urea nitrogen level, and the stress-induced hyperglycemia was significantly prevented by either phentolamine (10 mg/kg) or atropine (1 and 10 mg/kg). Plasma norepinephrine and epinephrine levels were also increased significantly by the stress, and the norepinephrine response was suppressed significantly by 6-hydroxydopamine. In conclusion, excessive peripheral sympathetic activity possibly plays an important role in the water immersion stress-induced increases in the plasma enzymes activity primarily via beta-adrenoceptors, whereas alpha-adrenoceptors and the cholinergic nerves might be involved in the stress-induced increases in plasma urea nitrogen and glucose levels.
Footnotes
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Send reprint requests to: Hiroshi Kodama, Ph. D., Division of Biological Sciences, Exploratory Research Laboratories, Tsukuba Research Laboratories, Fujisawa Pharmaceutical Co., Ltd., 5–2-3 Tokodai, Tsukuba, Ibaraki 300–26, Japan.
- Abbreviations:
- CPK
- creatine phosphokinase
- LDH
- lactic dehydrogenase
- GOT
- glutamic-oxalacetic transaminase
- GPT
- glutamic-pyruvic transaminase
- 6-OHDA
- 6-hydroxydopamine
- NE
- norepinephrine
- EPI
- epinephrine
- ANOVA
- analysis of variance
- HPLC
- high-performance liquid chromatography
- Received April 30, 1996.
- Accepted November 20, 1996.
- The American Society for Pharmacology and Experimental Therapeutics
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