THE PORTAL HYPERTENSIVE RESPONSE TO BRADYKININ IS MEDIATED BY THE B2-TYPE RECEPTOR AND MODULATED BY NITRIC-OXIDE

Using the in situ perfusion of the isolated and exsanguinated rat liver we studied: (1) the effect of des-Arg(9)[Leu(8)]-bradykinin and HOE-140, B1- and B2-type bradykinin receptor antagonists, respectively, on the portal hypertensive response (PHR) to bradykinin (BK) or to kallidin (Lys-BK); and (2) the effect of Nw-nitro-L-arginine (NNLA), a nitric oxide synthase inhibitor, on the PHR to BK. We observed that: (1) des-Arg(9)[Leu(8)]-BK does not change the PHR either to BK or to Lys-BK; (2) HOE-140 abolishes the PHR to both BK and Lys-BK; and (3) the presence of NNLA increases the PHR to BK. We conclude that the PHR to BK is mediated by the B2-type receptor and that this response is modulated by NO, which maintains a vasodilatory tonus on the portal system.