Key result
A1AR-deficiency did not result in significant phenotypic modifications on blood pressure, heart rate, and plasma renin across different genetic backgrounds (C57Bl/6 vs SWR/J).
Why the study?
Does A1AR-deficiency affect blood pressure, heart rate, and plasma renin differently depending on genetic background in mice?
Does A1AR-deficiency affect blood pressure, heart rate, and plasma renin differently depending on genetic background in mice?
Answers are grounded in this paper and cite their sources.
Genetic background differences between C57Bl/6 and SWR/J mice do not modify the phenotypic effects of A1AR-deficiency on blood pressure, heart rate, and plasma renin.
AIM: Differences in genetic background between control mice and mice with targeted gene mutations have been recognized as a potential cause for phenotypic differences. In this study, we have used A1AR-deficient mice in a C57Bl/6 and SWR/J congenic background to assess the influence of background on the effect of A1AR-deficiency on cardiovascular and renal functional parameters. METHODS: In A1AR+/+ and A1AR-/- mice in C57Bl/6 and SWR/J congenic backgrounds, we assessed blood pressure and heart rate using radio-telemetry, plasma renin concentrations and tubuloglomerular feedback. RESULTS: We did not detect significant differences in arterial blood pressure (MAP) and heart rates (HR) between A1AR+/+ and A1AR-/- mice in either C57Bl/6, SWR/J or mixed backgrounds. MAP and HR were significantly higher in SWR/J than in C57Bl/6 mice. A high NaCl intake increased MAP in A1AR-/- mice on C57Bl/6 background while there was less or no salt sensitivity in the SWR/J background. No significant differences in plasma renin concentration were detected between A1AR-/- and A1AR+/+ mice in any of the strains. Tubuloglomerular feedback was found to be absent in A1AR-/- mice with SWR/J genetic background. CONCLUSIONS: While this study confirmed important differences between inbred mouse strains, we did not identify phenotypic modifications of A1AR-related effects on blood pressure, heart rate and plasma renin by differences in genetic background.
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Kim et al. (2014) studied A1AR-deficiency. A1AR-deficiency vs. A1AR+/+ (wild type) was evaluated on Arterial blood pressure, heart rate, plasma renin concentrations, and tubuloglomerular feedback. A1AR-deficiency did not result in significant phenotypic modifications on blood pressure, heart rate, and plasma renin across different genetic backgrounds (C57Bl/6 vs SWR/J).
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