Blood pressure, heart rate and tubuloglomerular feedback in A1AR-deficient mice with different genetic backgrounds

Acta Physiol (Oxf). 2015 Jan;213(1):259-67. doi: 10.1111/apha.12377. Epub 2014 Sep 24.

Abstract

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.

Keywords: C57Bl/6 mice; SWR/J mice; adenosine; blood pressure telemetry; micropuncture.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Blood Pressure / genetics
  • Blood Pressure / physiology*
  • Glomerular Filtration Rate / genetics
  • Glomerular Filtration Rate / physiology
  • Heart Rate / genetics
  • Heart Rate / physiology*
  • Kidney / metabolism*
  • Mice, 129 Strain
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptor, Adenosine A1 / deficiency
  • Receptor, Adenosine A1 / metabolism*
  • Renin / metabolism

Substances

  • Receptor, Adenosine A1
  • Renin