In mice lacking the bradykinin-B2 receptor, an 8-week high-salt diet significantly increased mean arterial pressure compared to a normal salt diet (115 vs 79 mm Hg; P<0.0001).
Does a high-salt diet increase blood pressure in mutant mice lacking the bradykinin-B2 receptor?
Bradykinin-B2 receptors are essential for preventing salt-sensitive hypertension, likely by maintaining renal blood flow during high salt intake.
Absolute Event Rate: 115% vs 79%
p-value: p=<.0001
Renal kinins release prostaglandins and nitric oxide via the B2 receptor, promoting diuresis and natriuresis; hence, they may also contribute significantly to blood pressure regulation. We hypothesized that mutant mice lacking the gene encoding for the bradykinin-B2 receptor (B2-KO) become hypertensive when placed on a long-term high-salt diet. To test this, B2-KO and control mice were placed on either a normal (0.2%) or high-Na+ diet (3.15% in food plus 1% saline as drinking water) for 8 weeks. Systolic blood pressure was determined during weeks 6 and 8 by a computerized tail-cuff system. At the end of the 8-week period, mice were anesthetized for determination of mean blood pressure, renal blood flow, and renal vascular resistance. In B2-KO mice maintained on high Na+, systolic blood pressure was 15 mm Hg higher than in knockout animals on normal Na+ (P < .01). In contrast, there was no difference in blood pressure in control mice fed either a normal or a high-Na+ diet. Consistent with the systolic blood pressure data, direct mean arterial pressure revealed that B2-KO mice on high Na+ were hypertensive (115 +/- 6 in B2-KO on high-Na+ diet versus 79 +/- 2.8 in B2-KO on normal Na+, P < .0001); renal blood flow was reduced by 20% (P < .05) and renal vascular resistance was doubled (P < .0001) compared with B2-KO mice on normal Na+. In contrast, control mice on high Na+ were normotensive and tended to have increased renal blood flow and decreased renal vascular resistance compared with control mice on a normal Na+ diet. These findings indicate that kinins play an important role in preventing salt-sensitive hypertension; this may be achieved by maintaining renal blood flow under conditions of high salt intake.
Alfie et al. (1997) studied Salt-sensitive hypertension. High-salt diet vs. Normal salt diet (0.2%) was evaluated on Mean arterial pressure (p=<.0001). In mice lacking the bradykinin-B2 receptor, an 8-week high-salt diet significantly increased mean arterial pressure compared to a normal salt diet (115 vs 79 mm Hg; P<0.0001).
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