Objective To investigate the effects of histamine receptor antagonists on vasoconstriction induced by electrical stimulation （ES） on posterior auricular nerve,and to explore the pre-and post-synaptic effects of symp...Objective To investigate the effects of histamine receptor antagonists on vasoconstriction induced by electrical stimulation （ES） on posterior auricular nerve,and to explore the pre-and post-synaptic effects of sympathetic histamine on the vasomotor responses of vascular smooth muscle in rabbit ear.Methods ES was applied to posterior auricular nerves of the whole rabbit ear at 10 Hz,20 Hz and 40 Hz,respectively.Besides,the whole ear was perfused with different histamine receptor antagonists under constant perfusion pressure,and the changes in the flow rate of perfusate were observed.Results The flow rate of venous outflow was decreased by ES at all the 3 frequencies.The ES-induced vasoconstriction at 20 Hz and 40 Hz could be partly inhibited by H1 receptor antagonist chlorpheniramine （P0.05） .After exhaustion of histamine in mast cells by pretreatment with specific mast cell degranulator compound 48/80,chlorpheniramine could still inhibit the ES-induced flow rate reduction.In contrast,H2 receptor antagonist cimetidine could enhance the 40-Hz ES-induced flow rate reduction （P 0.05） .Moreover,ES-induced vasoconstriction at the 3 frequencies could all be enhanced by H3 receptor antagonist thioperamide （P0.05） .Conclusion Stimulation on the auricular nerve may evoke histamine release from sympathetic nerves rather than from mast cells.Moreover,the functions of sympathetic histamine vary from pre-synaptic modulation to post-synaptic vasoconstriction or vasodilatation,via activation of different histamine receptors.展开更多
Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovascular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine(NE) tran...Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovascular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine(NE) transporter(NET) on presynaptic membrane is a predominant component to eliminate released NE in the synaptic cleft and maintains the sensitivity of the β-adrenergic receptor(β-AR). In the present study,we investigated NET and β1-AR mRNA levels and sympathetic nerve density in cardiac sympathetic ganglion and left ventricular myocardium in 2-and 16-month-old rats with Northern blot analysis and immunohistochemistry. The expression levels of NET mRNA,NET protein and β1-AR mRNA in the ganglia or myocardia of 16-month-old rats were markedly reduced by 67%,26%,and 43%,respectively,in comparison with those in 2-month-old rats. Our results also show that aging induces a strong decrease of the catecholaminergic nerve fiber density.展开更多
基金supported by the National Natural Science Foundation of China(No.30770669,30800310)
文摘Objective To investigate the effects of histamine receptor antagonists on vasoconstriction induced by electrical stimulation （ES） on posterior auricular nerve,and to explore the pre-and post-synaptic effects of sympathetic histamine on the vasomotor responses of vascular smooth muscle in rabbit ear.Methods ES was applied to posterior auricular nerves of the whole rabbit ear at 10 Hz,20 Hz and 40 Hz,respectively.Besides,the whole ear was perfused with different histamine receptor antagonists under constant perfusion pressure,and the changes in the flow rate of perfusate were observed.Results The flow rate of venous outflow was decreased by ES at all the 3 frequencies.The ES-induced vasoconstriction at 20 Hz and 40 Hz could be partly inhibited by H1 receptor antagonist chlorpheniramine （P0.05） .After exhaustion of histamine in mast cells by pretreatment with specific mast cell degranulator compound 48/80,chlorpheniramine could still inhibit the ES-induced flow rate reduction.In contrast,H2 receptor antagonist cimetidine could enhance the 40-Hz ES-induced flow rate reduction （P 0.05） .Moreover,ES-induced vasoconstriction at the 3 frequencies could all be enhanced by H3 receptor antagonist thioperamide （P0.05） .Conclusion Stimulation on the auricular nerve may evoke histamine release from sympathetic nerves rather than from mast cells.Moreover,the functions of sympathetic histamine vary from pre-synaptic modulation to post-synaptic vasoconstriction or vasodilatation,via activation of different histamine receptors.
基金supported by the Postdoctoral Fellow Foundation of the Science and Technology Committee of Shanghai (No. 98-10)the Natural Science Foundation of Chinese People's Armed Police Force (Nos. WKH2006-5 and WKH2008ZO4), China
文摘Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovascular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine(NE) transporter(NET) on presynaptic membrane is a predominant component to eliminate released NE in the synaptic cleft and maintains the sensitivity of the β-adrenergic receptor(β-AR). In the present study,we investigated NET and β1-AR mRNA levels and sympathetic nerve density in cardiac sympathetic ganglion and left ventricular myocardium in 2-and 16-month-old rats with Northern blot analysis and immunohistochemistry. The expression levels of NET mRNA,NET protein and β1-AR mRNA in the ganglia or myocardia of 16-month-old rats were markedly reduced by 67%,26%,and 43%,respectively,in comparison with those in 2-month-old rats. Our results also show that aging induces a strong decrease of the catecholaminergic nerve fiber density.
