EFFECTS OF THYROTROPIN-RELEASING-HORMONE ON MYOCARDIAL ADRENOCEPTORS AND DOPAMINERGIC RECEPTORS FOLLOWING HEMORRHAGIC-SHOCK IN THE RAT

Although studies have indicated that thyrotropin-releasing hormone (TR H) produces various beneficial effects following low flow conditions, it remains unknown whether this agent has any salutary effect on myoca rdial alpha- and beta-adrenergic and dopaminergic (DA) receptors follo wing 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 p reparations at 15 and 45 min after TRH administration. The results ind icate that the maximal binding capacity (B-max) of myocardial alpha- a nd beta-adrenergic receptors and their affinity decreased significantl y following hemorrhage. The B-max of DA receptors was also reduced, wh ile 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 h emorrhage, however, markedly increased the B-max of myocardial beta-ad renergic and DA receptors. The decreased affinity of beta-adrenoceptor s observed in hemorrhaged animals was also improved with TRH treatment . TRH did not, however, significantly affect the altered B-max and aff inity of alpha-adrenoceptors following hemorrhagic shock. These result s suggest that TRH-induced upregulation of beta-adrenoceptor and DA re ceptor binding capacity and the enhanced affinity of beta-adrenoceptor s may be one of the mechanisms by which TRH produces the beneficial ef fects following hemorrhagic shock.