Key result
The l-NAME-induced mean arterial blood pressure increase during the day was smaller in RGS2-deficient mice compared to wild-type controls (11 +/- 1 vs. 17 +/- 2 mmHg; P < 0.05).
Why the study?
Does l-NAME treatment affect blood pressure and heart rate differently in RGS2-deficient mice compared to wild-type mice?
Does l-NAME treatment affect blood pressure and heart rate differently in RGS2-deficient mice compared to wild-type mice?
Absolute Event Rate: 11% vs 17%
p-value: p=<0.05
RGS2 deficiency blunts the l-NAME-induced blood pressure increase during the day, suggesting an interaction between RGS2 and the NO-cGMP pathway in blood pressure regulation.
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RGS2 deficiency blunts daytime BP response to NOS inhibition in mice; hypothesis-generating for RGS2-NO interactions, no clinical translation yet.
Obst et al. (2005) studied RGS2-deficient mice. l-NAME vs. RGS2(+/+) mice was evaluated on l-NAME-induced mean arterial blood pressure (MAP) increase during the day (p=<0.05). The l-NAME-induced mean arterial blood pressure increase during the day was smaller in RGS2-deficient mice compared to wild-type controls (11 +/- 1 vs. 17 +/- 2 mmHg; P < 0.05).
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