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Am J Physiol Renal Physiol 281: F665-F673, 2001;
0363-6127/01 $5.00
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Vol. 281, Issue 4, F665-F673, October 2001

Genetic disruption of atrial natriuretic peptide receptor-A alters renin and angiotensin II levels

Shang-Jin Shi, Huong T. Nguyen, Guru Dutt Sharma, L. Gabriel Navar, and Kailash N. Pandey

Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112

We have studied cardiovascular and renal phenotypes in Npr1 (genetic determinant of natriuretic peptide receptor-A; NPRA) gene-disrupted mutant mouse model. The baseline systolic arterial pressure (SAP) in 0-copy mutant (-/-) mice (143 ± 2 mmHg) was significantly higher than in 2-copy wild-type (+/+) animals (104 ± 2 mmHg); however, the SAP in 1-copy heterozygotes (+/-) was at an intermediate value (120 ± 4 mmHg). To determine whether Npr1 gene function affects the renin-angiotensin-aldosterone system (RAAS), we measured the components of RAAS in plasma, kidney, and adrenal gland of 0-copy, 1-copy, and 2-copy male mice. Newborn (2 days after the birth) 0-copy pups showed 2.5-fold higher intrarenal renin contents compared with 2-copy wild-type counterparts (0-copy 72 ± 12 vs. 2-copy 30 ± 7 µg ANG I · mg protein-1 · h-1, respectively). The intrarenal ANG II level in 0-copy pups was also higher than in 2-copy controls (0-copy 33 ± 5 vs. 2-copy 20 ± 2 pg/mg protein, respectively). However, both young (3 wk) and adult (16 wk) 0-copy mutant mice showed a dramatic 50-80% reduction in plasma renin concentrations (PRCs) and in expression of renal renin message compared with 2-copy control animals. In contrast, the adrenal renin content and mRNA expression levels were 1.5- to 2-fold higher in 0-copy adult mice than in 2-copy animals. The results suggest that inhibition of renal and systemic RAAS is a compensatory response that prevents greater increases in elevated arterial pressures in adult NPRA null mutant mice. However, the greater renin and ANG II levels seen in 0-copy newborn pups provide evidence that the direct effect of NPRA activation on renin is an inhibitory response.

guanylyl cyclase A; gene targeting; renin-angiotensin-aldosterone system; renin activity; natriuretic peptide receptor-A gene-deficient mice


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