Key result
ANP gene disruption in mice resulted in lower renal and adrenal renin mRNA and angiotensin II levels, higher renal arterial pressure, and a blunted acute pressure-natriuresis response.
ANP gene disruption in mice leads to a blunted acute pressure-natriuresis mechanism and altered local renin-angiotensin system expression, contributing to the understanding of salt-sensitive hypertension.
ANP deficiency alters renal renin-angiotensin and pressure-natriuresis in mice; leaves open relevance to human salt-sensitive hypertension.
BACKGROUND: Although it has been well established that atrial natriuretic peptide gene-disrupted (ANP-/-) mice are a useful model of salt-sensitive hypertension, surprisingly little is known about the control of their intrarenal renin-angiotensin system (RAS) and pressure-natriuresis mechanism, key components in blood pressure, fluid and electrolyte regulation. The aim of this study was to determine whether ANP disruption results in changes in the renal and adrenal local RAS and the acute pressure-natriuresis mechanism. METHODS: Renal and adrenal renin, angiotensin type 1 (AT1)(A and B) and angiotensin type 2 (AT2) receptor messenger RNA expression levels were determined by northern blotting or real time reverse transcriptase-polymerase chain reaction. Plasma aldosterone and renal and adrenal angiotensin II peptide levels were determined by radioimmunoassay. To examine the acute pressure-natriuresis response, changes in renal interstitial hydrostatic pressure (RIHP) were assessed after manipulations of renal arterial pressure (RAP) in anaesthetized mice. RESULTS: Renal and adrenal renin mRNA and angiotensin II levels were lower in ANP-/- and +/- mice compared with +/+mice. ANP-/- mice also had greater renal AT1A and adrenal AT2 mRNA levels compared with the other genotypes. RAP and RIHP were significantly higher in -/-mice compared with +/+mice. Furthermore, there was a blunted slope of the RAP-RIHP relationship after increases in RAP in ANP-/- mice. CONCLUSION: These data indicate that ANP disruption results in a blunting of the dynamic properties of the acute pressure-natriuresis mechanism at increased levels of RAP, as well as a reduced expression of renal and adrenal local RAS.
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O’Tierney et al. (2008) studied Salt-sensitive hypertension model. Atrial natriuretic peptide (ANP) gene disruption vs. Wild-type (+/+) and heterozygous (+/-) mice was evaluated on Renal and adrenal renin mRNA, angiotensin II levels, and acute pressure-natriuresis response. ANP gene disruption in mice resulted in lower renal and adrenal renin mRNA and angiotensin II levels, higher renal arterial pressure, and a blunted acute pressure-natriuresis response.
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