With inhibition or absence of the B₂ receptor of bradykinin, the B₁ receptor is upregulated and assumes some of the hemodynamic properties of the B₂ receptor, indicating that both participate in the maintenance of normal vasoregulation or to development of hypertension. The current experiments were designed to further evaluate the role of bradykinin in normal blood pressure (BP) regulation and its relationship with other vasoactive factors by selectively blocking its receptors. Six groups of Wistar rats were treated for a period of three weeks: one control group with vehicle solution alone, one with concurrent administration of the B₁ antagonist R-954 (70 µg/kg/d) and the B₂ antagonist HOE 140 (500 µg/kg/d), one with the B₁ antagonist alone, one with the B₂ antagonist alone, one with concurrent administration of both the B₁ and B₂ antagonists plus the angiotensin antagonist losartan (5 mg/kg/day), and one with only losartan. BP was measured continuously during this period via a telemetry system. Only the combined administration of B₁ and B₂ receptor antagonist produced a significant BP increase from a baseline of 107 to 119 mmHg at endpoint, which could be partly prevented by losartan and was not associated with change in catecholamines, suggesting no involvement of the sympathoadrenal system. The impact of blockade of bradykinin on other vasoregulating systems was assessed by evaluating gene expression of different vasoactive factors: there was upregulation of the eNOS, AT₁ receptor, PGE2 receptor, and KLK genes in cardiac and renal tissues, more pronounced when both bradykinin receptors were blocked, significant downregulation of AT₂ receptor gene in renal tissues only and no consistent changes in B₁ and B receptor genes in either tissue. The results indicate that both bradykinin receptors contribute to the maintenance of normal BP, but one can compensate for inhibition of the other and the chronic inhibition of both leads to significant upregulation in the genes of related vasoactive systems.