This project was designed to elucidate the integrative role of bradykinin (B2)receptors, in the interaction with renin angiotensin system (RAS) and its possible impact on the development of angiotensin II-induced hypertension in Cre/lox mice for B2 receptor gene (BRAD) in the distal tubule. Radiotransmitters (TA11PA-C10, Data Science Internatinal) were implanted in anesthetized mice (tiletamine, zolazepam, 8 mg/kg and xylazine, 4 mg/kg, intramuscular administration) as follow: a midline skin incision 2 cm long from chin to manubrium is performed to isolate the common carotid artery. A blunt trocar is passed from the neck incision to abdominal region through the lateral aspect under the skin. The catheter of the implant is introduced via common carotid artery to the aortic arch. The transmitter body is placed under the skin in the abdominal region and the skin is sutured. After 8-10 days of recovery, the monitoring is initiated continuously using the telemetry data acquisition system.In 3 groups of lox BRAD mice and 3 groups of Cre/lox BRAD conditional knockout mice, salt-sensitive component of this model was tested in mice fed high salt diets (4 or 8% NaCl) for 2 weeks in comparison with standard salt diet (0.4%). Hypertension was induced by angiotensin II administration (1000 ng/min/kg) via osmotic minipumps (Alzet 1002) implanted subcutaneously. At the end of the protocol, the animals were euthanized by anesthetic overdose to collect the tissue samples. We observed that none of the high salt intake causes a rise in systolic blood pressure (SBP) in both lox BRAD (119 ± 2 to 121 ± 3 mmHg) and Cre/lox BRAD mice (118 ± 2 to 124 ± 4 mmHg). Angiotensin II chronic infusion significantly increased SBP similarly in both lox BRAD (121 ± 2 to 156 ± 3 mmHg) and Cre/lox BRAD mice (120 ± 2 to 153 ± 2 mmHg) strains. Although, 4 % high salt intake exacerbated the development of angiotensin II-induced hypertension in both lox BRAD (125 ± 3 to 164 ± 5 mmHg) and Cre/lox BRAD mice (124 ± 2 to 162 ± 3 mmHg) strains during 2 weeks in the same manner, 8 % salt intake in Cre/lox BRAD mice further accelerated the rise of the blood pressure (129 ± 3 to 165 ± 4 mmHg) within 1 week compare to lox BRAD control (128 ± 2 to 159 ± 3 mmHg). This rapid progression of hypertension was accompanied by body weight loss and increased mortality. In conclusion, conditional inactivation of B2 receptors in the distal tubule did not cause salt-sensitivity. However, it seems that B2 receptors attenuate the action of the RAS in the regulation of sodium handling under very high salt condition and hypertension.