サブスタンスP及びヒスタミン遊離におけるヒスタミンH_3受容体を介するnegative feedback機構について
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Role of histamine H_3-receptors on the regulation of release of substance P (SP) and histamine in neurogenic inflammation was investigated. (R)^α-methylhistamine (MeHA) (0.5-3 mg/kg, i. v.), a specific H_3-agonist, significantly inhibited the increased vascular permeability induced by antidromic electric stimulation of the sciatic nerve in the rat hindpaw in a dose-related manner, and thioperamide (Thio) (3 mg/kg, i. p.), a specific H_3-antagonist, antagonized it. MeHA (O.25-2 mg/kg, i. v.) caused a significant dose-dependent inhibition of the increase in release of immunoreactive SP (i-SP) and histamine in the subcutaneous (s. c. ) perfusate in the rat hindpaw induced by antidromic stimulation, and Thio (2 mg/kg, i. p. ) prevented the inhibitory effect of MeHA. Perfusion of histamine (10^<_3>M) led to a significant increase of i-SP in the s. c. perfusate, which was inhibited by MeHA (1 mg/kg) , and Thio (2 mg/kg) reduced the response to MeHA. On the other hand, perfusion of SP (2.5×10^<-5>M) elicited a significant increase of histamine in the perfusate. The inhibitory action of MeHA and the antagonism of Thio on the histamine release were also observed. MeHA (5,50μg/ml) also inhibited histamine release by SP (3μg/ml) from rat peritoneal mast cells in vitro, and Thio (5μg/ml) antagonized it. Glibenclamide (10 mg/kg, i. v. ) , a ATP-sensitive K^+ channel blocker, abolished the response to MeHA (1 mg/kg) on the release of i-SP and histamine. The increase in i-SP release in the s. c. perfusate by antidromic stimulation or histamine stimulation was inhibited by mepyramine (5 mg/kg, i. p. ), an H_1-antagonist, but not by cimetidine (5 mg/kg, i. p. ), an H_2-antagonist. These results suggest that histamine may prevent the release of SP and histamine via H_3-receptors which may exist in both sites of peripheral sensory nerve endings and mast cells, and ATP-sensitive K^+ channel may be involved in the inhibitory action of H_3-receptors. Furthermore, H_1-receptors may also exist in nerve endings and be involved in SP release.
- 福岡歯科大学学会の論文
- 1994-06-30
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