Although studies have indicated that thyrotropin-releasing hormone (TRH) produces various beneficial effects following low flow conditions, it remains unknown whether this agent has any salutary effect on myocardial alpha- and beta-adrenergic and dopaminergic (DA) receptors following hemorrhagic shock. To study this, rats (220-280 g) were bled to a mean arterial pressure of 40 mmHg and maintained for 1.5 h following shock. TRH or an equivalent volume of normal saline was administered. Receptor binding assay was carried out in myocardial plasma membrane preparations at 15 and 45 min after TRH administration. The results indicate that the maximal binding capacity (Bmax) of myocardial alpha- and beta-adrenergic receptors and their affinity decreased significantly following hemorrhage. The Bmax of DA receptors was also reduced, while the affinity was not significantly affected by hemorrhagic insult. Administration of TRH (5 mg/kg body wt) at 1.5 h after the onset of hemorrhage, however, markedly increased the Bmax of myocardial beta-adrenergic and DA receptors. The decreased affinity of beta-adrenoceptors observed in hemorrhaged animals was also improved with TRH treatment. TRH did not, however, significantly affect the altered Bmax and affinity of alpha-adrenoceptors following hemorrhagic shock. These results suggest that TRH-induced upregulation of beta-adrenoceptor and DA receptor binding capacity and the enhanced affinity of beta-adrenoceptors may be one of the mechanisms by which TRH produces the beneficial effects following hemorrhagic shock.