Nitric oxide and its role in the induction of kinin B(1)-receptors after heat stress in the rat.

Kinin B(1)-receptors are inducible-receptors. They are absent under basal conditions but expressed following pathophysiological stresses. This study was designed to examine a possible role of nitric oxide (NO) in the mechanism underlying B(1)-receptor induction after heat stress (HS). Rats were divided into six groups, subjected or not to HS (42 degrees C internal temperature, 20 min) without or with treatment with nitro-L-arginine-methylester (L-NAME), a nonselective inhibitor of NO synthase (NOS) isoforms, or L-N(6)-(1-imino-ethyl)lysine (L-NIL), a selective inhibitor of the inducible NOS. Twenty-four hours after HS, rats were injected with bradykinin and [des-Arg(9)]-bradykinin and hypotensive responses were recorded. In six additional groups, B(1)-receptor mRNAs were detected in aorta 5 h after HS or sham treatment. Bradykinin, a B(2)-receptor agonist, induced a hypotension of a similar magnitude in all the groups studied. [des-Arg(9)]-bradykinin, a B(1)-receptor agonist, induced no response in sham rats. In rats previously subjected to hyperthermia, this agonist induced a hypotensive response, which was, respectively, decreased and increased by pretreatment with L-NAME and with L-NIL prior to hyperthermia. RT-PCR results confirmed these in vivo observations. In conclusion, this study suggests a role for NO in B(1)-receptor induction after HS as well as a possible interaction between NOS isoforms.