Bradykinin-mediated edema formation is blocked by levorotatory but not dextrorotatory terbutaline.

The ability of the purified stereoisomers of the beta 2-receptor agonist terbutaline to block bradykinin-mediated increases in lymph flow and protein concentration was assessed in the canine forelimb perfused at constant arterial flow. Intra-arterial infusion of bradykinin (2 micrograms/min, n = 8) decreased forelimb arterial pressures but did not affect skin small vein pressure or systemic pressure. Lymph flow, protein concentration and protein transport were significantly increased. Intra-arterial infusion of 1-terbutaline (1 microgram/min, n = 9) decreased forelimb arterial pressures and systemic pressure but did not affect lymph parameters. Subsequent infusion of bradykinin during the continued infusion of 1-terbutaline failed to alter forelimb lymph parameters. Intra-arterial infusion of d-terbutaline (1 microgram/min, n = 11) did not alter vascular pressures or lymph parameters. Subsequent infusion of bradykinin during the continued infusion of d-terbutaline decreased forelimb arterial pressures and significantly increased lymph flow, protein concentration and protein transport. Intra-arterial infusion of a high dose (100 micrograms/min, n = 9) of d-terbutaline significantly decreased forelimb arterial pressure but was likewise ineffective in blocking the increases in lymph parameters produced by subsequent bradykinin infusion. These data indicate that the beta 2-receptor agonistic and anti-permeability actions of terbutaline are found solely in the levorotatory enantiomer.