Heat stress-induced B1 receptor synthesis in the rat: an ex vivo study.

Abstract

1. This ex vivo study was performed to characterize B1 receptor induction in rats submitted to heat stress. Changes in aortic isometric tension were recorded after a 90 min in vitro incubation with [des-Arg9]-bradykinin. B1 receptor mRNA were detected in aorta and heart using RT-PCR technique. 2. Aortic rings from sham rats did not respond to [des-Arg9]-bradykinin. In contrast, this agonist induced a concentration-dependent relaxation of aortic rings from rats submitted to lipopolysaccharide (LPS) treatment or to heat stress 24 h earlier. 3. The concentration-dependent relaxation induced by [des-Arg9]-bradykinin on aortic rings from heat-stressed rats was abolished by [des-Arg10]-HOE 140, a selective B1 receptor antagonist. 4. In endothelium denuded aortic rings from heat-stress rats, [des-Arg9]-bradykinin induced a concentration-dependent constriction. 5. Pretreatment of intact aortic rings from heat-stress rats with the cyclo-oxygenase inhibitor, diclofenac (1 microM) did not prevent the concentration-dependent relaxation in response to [des-Arg9]-bradykinin. In contrast. NO synthase inhibition with N(omega)-nitro-L-arginine methyl ester (30 microM) totally prevented the vasorelaxant response. 6. B1 receptor mRNA were not detected in aorta and heart from sham animals but were present in tissue from heat-stressed and LPS-treated rats. 7. In conclusion, our results suggest that heat stress induces a transcriptional activation of the B1 receptor gene. The induction of B1 receptors leads to an endothelium- and NO-dependent vasorelaxant response to [des-Arg9]-bradykinin.