Abstract

The effect of various adrenergic drugs on the free fatty acid (FFA) output from bone marrow was studied in dog tibia after constant flow autoperfusion of the nutrient artery by femoral arterial blood and cannulation of the nutrient vein. Clonidine, an alpha-2 adrenoceptor agonist, inhibited the isoproterenol-induced FFA outflow from bone marrow adipose tissue. This effect was suppressed by the alpha-2 antagonists (phentolamine and yohimbine). Moreover, clonidine inhibited the FFA outflow initiated by theophylline associated with adenosine deaminase. When the alpha-2 sites were blocked by phentolamine or yohimbine, epinephrine exerted an enhanced effect on FFA outflow in comparison with its effect when infused alone. These in vivo experiments clearly demonstrate that alpha-2 adrenoceptor stimulation is able to inhibit beta-stimulated or theophylline plus adenosine deaminase-promoted lipid mobilization from bone marrow fat stores. The simultaneous stimulation of alpha-2 and beta adrenoceptors initiated by epinephrine could be responsible for the weaker lipid-mobilizing effect of the endogenous catecholamine. It is concluded that adrenoceptors are operative in bone marrow adipose tissue and control FFA outflow in physiological conditions. Moreover, the existence of an interplay between alpha-2 and beta adrenergic effects in in vivo conditions is demonstrated.