Histamine H1- and H2-receptors participate to provide metabolic energy differently.

Abstract

Histamine participates in a variety of physiological functions. The local effects of histamine have a role to provide metabolic energy for the tissues. The objective of this work is to study the mechanism whereby histamine affects serum glucose and liver glycogen fractions. Six groups of 10 male rats received two injections with histamine, H1-agonist (dipyridylethylamine), H2-agonist (dimaprit), H1-agonist plus H1-antagonist (cetirizine), or H2-agonist plus H2-antagonist (famotidine). Serum glucose and liver glycogen fractions were measured. Histamine caused a significant increase in serum glucose (163.7±5.4 vs. 153.2±3.3mg/dl, p= 0.023). The effect of histamine was mimicked by selective H1-agonist (164.2±3.5 vs. 152.8±2.9mg/dl, p= 0.005) but not with H2-agonist (159.3±3.7 vs. 156.3±4.8mg/dl, p= 0.281). The effect of H1-agonist was abolished in the presence of selective H1-antagonist. Treatment by H1- but not H2-agonist decreased total glycogen by about 35% (30.6±0.5 vs. 47.3±2.8mg/g wet weight of liver, p= 0.003). The decrease happened wholly in ASG fraction (26.8±1.2 vs. 43.7±3.2mg/g wet weight of liver, p= 0.004), while AIG did not change significantly (4.2±0.5 vs. 4.5±0.4mg/g wet weight of liver, p= 0.724). Histamine causes to decrease glycogen in the liver and increased serum glucose. The effects of histamine were mediated via H1-receptors. ASG was metabolically active fraction of liver glycogen in this process. The results confirm the role of histamine in providing metabolic energy of the tissues.