Background:In this study we compared the effect of bradykinin (BK) on insulin-receptor interaction in rat adipose plasma membranes under normothermic and hypothermic conditions.
Material/Methods: Plasma membranes were prepared and purified according to Havrankova and binding assay was performed using ([sup]125[/sup]I) – insulin. The kinetic parameters of the hormone-receptor interaction were analyzed according to Scatchard using the LIGAND – Pc v.3.1 computer program. Additionally, we determined blood glucose and insulin concentrations. The results were interpreted statistically according to one-way analysis of variance (ANOVA).Results: Statistically significant changes mainly involved the low-affinity receptor class. In normothermic rats, BK provoked a decrease in insulin-receptor affinity (expressed as a drop in the association constant Ka2 by 64% and enhancement in the dissociation constant Kd2 by 215%), which was compensated by a 188% increase in the number of insulin receptors. Therefore, association constant times binding capacity remained unchanged. Administration of BK resulted in a decrease in serum glucose concentration by about 50%, while the insulin level did not change. Hypothermia lowered insulin concentration by 68% and elevated both the value of the association constant times binding capacity by 166% and the insulin-receptor affinity (Kd2 decreased by 71% and Ka2 increased markedly by about 771%). Administration of BK to hypothermic rats elevated blood insulin level by 180% and diminished (by about 64%) the value of association constant times binding capacity.Conclusions: The results indicate that bradykinin plays a significant role in carbohydrate metabolism and may influence insulin-receptor interaction under both normothermic and hypothermic conditions.

Keywords: Adipose Tissue - drug effects, Adipose Tissue - metabolism, Bradykinin - pharmacology, Cell Membrane - drug effects, Cell Membrane - metabolism, Hypothermia, Induced, Insulin - metabolism, Receptor, Insulin - metabolism, Adipose Tissue - metabolism, Bradykinin - pharmacology, Cell Membrane - metabolism, Hypothermia, Induced, Insulin - metabolism, Receptor, Insulin - metabolism