AJP - Renal AJP: Advances in Physiology Education
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 281: F665-F673, 2001;
0363-6127/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (20)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Shi, S.-J.
Right arrow Articles by Pandey, K. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Shi, S.-J.
Right arrow Articles by Pandey, K. N.
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


This article has been cited by other articles:


Home page
 Physiol. GenomicsHome page
E. Vellaichamy, D. Zhao, N. Somanna, and K. N. Pandey
Genetic disruption of guanylyl cyclase/natriuretic peptide receptor-A upregulates ACE and AT1 receptor gene expression and signaling: role in cardiac hypertrophy
Physiol Genomics, October 19, 2007; 31(2): 193 - 202.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
D. Zhao, E. Vellaichamy, N. K. Somanna, and K. N. Pandey
Guanylyl cyclase/natriuretic peptide receptor-A gene disruption causes increased adrenal angiotensin II and aldosterone levels
Am J Physiol Renal Physiol, July 1, 2007; 293(1): F121 - F127.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Coll. Nutr.Home page
V. Franco and S. Oparil
Salt sensitivity, a determinant of blood pressure, cardiovascular disease and survival.
J. Am. Coll. Nutr., June 1, 2006; 25(3 Suppl): 247S - 255S.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
L. J. Mullins, M. A. Bailey, and J. J. Mullins
Hypertension, Kidney, and Transgenics: A Fresh Perspective
Physiol Rev, April 1, 2006; 86(2): 709 - 746.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
Y. Ge, D. Ahn, P. K. Stricklett, A. K. Hughes, M. Yanagisawa, J. G. Verbalis, and D. E. Kohan
Collecting duct-specific knockout of endothelin-1 alters vasopressin regulation of urine osmolality
Am J Physiol Renal Physiol, May 1, 2005; 288(5): F912 - F920.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
T. Nishikimi, J. R. Hagaman, N. Takahashi, H.-S. Kim, H. Matsuoka, O. Smithies, and N. Maeda
Increased susceptibility to heart failure in response to volume overload in mice lacking natriuretic peptide receptor-A gene
Cardiovasc Res, April 1, 2005; 66(1): 94 - 103.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
S.-J. Shi, E. Vellaichamy, S. Y. Chin, O. Smithies, L. G. Navar, and K. N. Pandey
Natriuretic peptide receptor A mediates renal sodium excretory responses to blood volume expansion
Am J Physiol Renal Physiol, October 1, 2003; 285(4): F694 - F702.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online