scholarly journals Small interfering RNA‐mediated functional silencing of natriuretic peptide receptor‐A in human embryonic kidney ‐293 cells

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Naveen K Somanna ◽  
Kiran K Arise ◽  
Edwin Wu ◽  
Kailash N Pandey
Keyword(s):  
Natriuretic Peptide ◽  
Small Interfering Rna ◽  
Natriuretic Peptide Receptor ◽  
Human Embryonic Kidney ◽  
Peptide Receptor ◽  
293 Cells ◽  
Natriuretic Peptide Receptor A ◽  
Interfering Rna

Physical Mapping of the Human Connexin 40 (GJA5), Flavin-Containing Monooxygenase 5, and Natriuretic Peptide Receptor A Genes on 1q21

Genomics ◽  
1997 ◽  
Vol 39 (3) ◽  
pp. 409-411 ◽  
Author(s):  
Bruce D. Gelb ◽  
Jian Zhang ◽  
Philip D. Cotter ◽  
Irina F. Gershin ◽  
Robert J. Desnick
Keyword(s):  
Natriuretic Peptide ◽  
Physical Mapping ◽  
Natriuretic Peptide Receptor ◽  
Peptide Receptor ◽  
Connexin 40 ◽  
Natriuretic Peptide Receptor A

Localization by Photoaffinity Labeling of Natriuretic Peptide Receptor-A Binding Domain†

Biochemistry ◽  
1996 ◽  
Vol 35 (39) ◽  
pp. 12950-12956 ◽  
Author(s):  
Normand McNicoll ◽  
Jean Gagnon ◽  
Jean-Jacques Rondeau ◽  
Huy Ong ◽  
André De Léan
Keyword(s):  
Natriuretic Peptide ◽  
Photoaffinity Labeling ◽  
Binding Domain ◽  
Natriuretic Peptide Receptor ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A

scholarly journals Molecular and genetic aspects of guanylyl cyclase natriuretic peptide receptor-A in regulation of blood pressure and renal function

2018 ◽  
Vol 50 (11) ◽  
pp. 913-928 ◽  
Author(s):  
Kailash N. Pandey
Keyword(s):  
Blood Pressure ◽  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Natriuretic Peptides ◽  
Molecular Mechanisms ◽  
Phenotypic Characterization ◽  
Natriuretic Peptide Receptor ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A ◽  
Regulation Of Blood Pressure

Natriuretic peptides (NPs) exert diverse effects on several biological and physiological systems, such as kidney function, neural and endocrine signaling, energy metabolism, and cardiovascular function, playing pivotal roles in the regulation of blood pressure (BP) and cardiac and vascular homeostasis. NPs are collectively known as anti-hypertensive hormones and their main functions are directed toward eliciting natriuretic/diuretic, vasorelaxant, anti-proliferative, anti-inflammatory, and anti-hypertrophic effects, thereby, regulating the fluid volume, BP, and renal and cardiovascular conditions. Interactions of NPs with their cognate receptors display a central role in all aspects of cellular, biochemical, and molecular mechanisms that govern physiology and pathophysiology of BP and cardiovascular events. Among the NPs atrial and brain natriuretic peptides (ANP and BNP) activate guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) and initiate intracellular signaling. The genetic disruption of Npr1 (encoding GC-A/NPRA) in mice exhibits high BP and hypertensive heart disease that is seen in untreated hypertensive subjects, including high BP and heart failure. There has been a surge of interest in the NPs and their receptors and a wealth of information have emerged in the last four decades, including molecular structure, signaling mechanisms, altered phenotypic characterization of transgenic and gene-targeted animal models, and genetic analyses in humans. The major goal of the present review is to emphasize and summarize the critical findings and recent discoveries regarding the molecular and genetic regulation of NPs, physiological metabolic functions, and the signaling of receptor GC-A/NPRA with emphasis on the BP regulation and renal and cardiovascular disorders.

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

2001 ◽  
Vol 281 (4) ◽  
pp. F665-F673 ◽  
Author(s):  
Shang-Jin Shi ◽  
Huong T. Nguyen ◽  
Guru Dutt Sharma ◽  
L. Gabriel Navar ◽  
Kailash N. Pandey
Keyword(s):  
Natriuretic Peptide ◽  
Systolic Arterial Pressure ◽  
Inhibitory Response ◽  
Mutant Mice ◽  
Natriuretic Peptide Receptor ◽  
Ang Ii ◽  
Wild Type ◽  
Compensatory Response ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A

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.

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