Exogenous catecholamines have been proved to be active in the reduction of vascular permeability induced by various inflammatory mediators via beta-adrenoceptor activation, but it is not known whether an endogenous beta-adrenergic agonist has any effect. We studied it in skin and lung vessels. The results revealed that an intravenous bolus of isoproterenol (10 micrograms/kg) attenuated platelet-activating factor- and histamine-induced Evans blue dye extravasation in rat dorsal skin, while intraperitoneal administration of beta-adrenoceptor blocker propranolol (0.1 mg/kg) significantly increased the dye extravasation. Blockade of beta-adrenoceptor by propranolol for 12 h noticeably increased wet/dry lung weight ratio, lung water content, bronchoalveolar lavage (BAL) protein concentration, leukocyte count, and lipoperoxide degradation product malondialdehyde (MDA) content. In isolated perfused lung in vitro, propranolol (2.5 micrograms/ml) had no obvious effects on lung weight gain, fluid filtration coefficient, and pulmonary vascular pressure during the 20-min perfusion compared with control. The results suggested that endogenous beta-adrenergic agonist is an important factor in the maintenance of vascular integrity and the quiescent state of leukocytes, indicating the antiinflammatory role of catecholamines in physiological states and critical illnesses.