Augmentation of BNP gene expression in atria by pressure overload in transgenic rats harbouring human renin and angiotensinogen genes

We studied the role of angiotensin II in pressure overload-induced B-type n atriuretic peptide (BNP) gene expression by using a double transgenic rat ( dTGR) model, in which transgenic rats for the human angiotensinogen and ren in genes are crossed. Pressure overload produced by [Arg(8)]-vasopressin (A VP) infusion (i.v., 0.05 mu g/kg/min for 2 h) in conscious, chronically ins trumented rats, resulted in a significantly greater increase in BNP mRNA le vels in the left atrium of the dTGR rats than in Sprague-Dawley (SD) contro l rats (3.6- us 1.6-fold, p < 0.05), while in the left ventricle there was no significant difference between the strains. In dTGR rats, the early acti vation of the BNP gene expression was associated with a decrease in immunor eactive BNP levels in the atrium (27.5%, p < 0.05), but not in thp ventricl e. In SD rats, ir-BNP levels did not change significantly in either atria o r ventricles in response to AVP infusion. These results show that the press ure overload-induced activation of BNP gene expression differs between atri al and ventricular myocytes in the dTGR model of experimental hypertension.