Bradykinin has vasodilatory and tissue-protective effects exerted via its B2type receptor, whereas the B1receptor is constitutively absent but inducible by inflammation and toxins. In previous studies, we found that B2receptor gene knockout mice exhibit overexpression of the B1receptor, which assumes a vasodilatory function and is further upgraded in renovascular hypertension. The present study was designed to explore the effects of excess angiotensin II (ANG II) on B1receptor and B2receptor gene expression in mouse cardiomyocytes and rat vascular smooth muscle cells (VSMC) in vivo (after a 3-day infusion of 30 ng/min ANG II in 11 wild-type and in 13 genetically engineered mice with deleted B2receptor gene) and in vitro (ANG II added in rat VSMC culture in the presence or absence of AT1or AT2receptor antagonist). Expression of B1and B2receptor mRNA was assessed by reverse transcriptase-polymerase chain reaction. ANG II infusion caused upregulation by 30% of the already significantly overexpressed B1receptors in cardiomyocytes of the B2receptor gene knockout mice, but in the wild-type mice it upregulated only the B2receptor mRNA by 47%. The addition of ANG II in VSMC culture produced a time-dependent induction of B1and upregulation of B2receptor gene expression, maximal at 3 h (by fivefold), declining almost to baseline by 24 h. The addition of losartan completely blocked this effect, whereas the AT2blocker PD-123319 made no difference, indicating that this is an AT1-mediated effect of ANG II. The data indicate that excess ANG II in subpressor doses in vivo upregulates expression of the B2receptor, but in its absence, the already overexpressed B1receptor is further upregulated, evidently assuming a counterregulatory response; in vitro, it transiently upregulates both bradykinin receptors.