scholarly journals Npr2 mutant mice show vasodilation and undeveloped adipocytes in mesentery

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Chizuru Sogawa-Fujiwara ◽  
Yasuhiro Fujiwara ◽  
Atsuki Hanagata ◽  
Qunhui Yang ◽  
Taiki Mihara ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Blood Vessels ◽  
Natriuretic Peptide ◽  
Mutant Mouse ◽  
Spontaneous Mutant ◽  
Natriuretic Peptide Receptor ◽  
Histological Observation ◽  
Peptide Receptor ◽  
Vascular Morphology

Abstract Objective The biological importance for the signaling of C-type natriuretic peptide (CNP) and natriuretic peptide receptor B (NPR-B) has been recognized. However, the details remain unclear and are debatable. The Npr2 is a gene of NPR-B, and we previously reported a unique phenotype of a spontaneous mutant mouse lacking Npr2 (Npr2slw/slw), such as severe ileus-like disorder with bloodless blood vessels. In this study, we analyzed the bloodless mesenteric vascular morphology of Npr2slw/slw by histological observation to clarify the effects of the CNP/NPR-B signal deficiency. Results Blood vessels in the mesentery were clearly dilated in the preweaning Npr2slw/slw mice. Additionally, in the Npr2slw/slw mice, the lacteals were partially dilation or randomly direction mucosal epithelial cells in villi, and mesenteric adipocytes were undeveloped. These findings provide important information for understanding the role of CNP/NPR-B signals on intestine with mesentery.

Role of Natriuretic Peptide Receptor Type C in Dahl Salt-Sensitive Hypertensive Rats

Hypertension ◽  
1997 ◽  
Vol 30 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Miki Nagase ◽  
Katsuyuki Ando ◽  
Takeshi Katafuchi ◽  
Akira Kato ◽  
Shigehisa Hirose ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Receptor Type ◽  
Natriuretic Peptide Receptor ◽  
Hypertensive Rats ◽  
Peptide Receptor ◽  
Type C

scholarly journals The Importance of Natriuretic Peptides in Cardiometabolic Diseases

2020 ◽  
Vol 4 (6) ◽  
Author(s):  
Shravya Vinnakota ◽  
Horng H Chen
Keyword(s):  
Heart Failure ◽  
Natriuretic Peptide ◽  
Defense Mechanisms ◽  
Pressure Overload ◽  
Natriuretic Peptide Receptor ◽  
Therapeutic Role ◽  
Peptide Receptor ◽  
Genes Encoding ◽  
Natriuretic Peptide Receptor A

Abstract The natriuretic peptide (NP) system is composed of 3 distinct peptides (atrial natriuretic peptide or ANP, B-type natriuretic peptide or BNP, and C-type natriuretic peptide or CNP) and 3 receptors (natriuretic peptide receptor-A or NPR-A or particulate guanynyl cyclase-A natriuretic peptide receptor-B or NPR-B or particulate guanynyl cyclase-B, and natriuretic peptide receptor-C or NPR-C or clearance receptor). ANP and BNP function as defense mechanisms against ventricular stress and the deleterious effects of volume and pressure overload on the heart. Although the role of NPs in cardiovascular homeostasis has been extensively studied and well established, much remains uncertain about the signaling pathways in pathological states like heart failure, a state of impaired natriuretic peptide function. Elevated levels of ANP and BNP in heart failure correlate with disease severity and have a prognostic value. Synthetic ANP and BNP have been studied for their therapeutic role in hypertension and heart failure, and promising trials are under way. In recent years, the expression of ANP and BNP in human adipocytes has come to light. Through their role in promotion of adipocyte browning, lipolysis, lipid oxidation, and modulation of adipokine secretion, they have emerged as key regulators of energy consumption and metabolism. NPR-A signaling in skeletal muscles and adipocytes is emerging as pivotal to the maintenance of long-term insulin sensitivity, which is disrupted in obesity and reduced glucose-tolerance states. Genetic variants in the genes encoding for ANP and BNP have been associated with a favorable cardiometabolic profile. In this review, we discuss several pathways that have been proposed to explain the role of NPs as endocrine networkers. There is much to be explored about the therapeutic role of NPs in improving metabolic milieu.

735 Role of P38 MAPK in aldosterone-induced glomerular injury in natriuretic peptide receptor-A deficient mice

2012 ◽  
Vol 30 (Supplement 1) ◽  
pp. e213
Author(s):  
Yukiko Kato ◽  
Masashi Mukoyama ◽  
Hideki Yokoi ◽  
Yoshihisa Ogawa ◽  
Kiyoshi Mori ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Natriuretic Peptide ◽  
Natriuretic Peptide Receptor ◽  
Glomerular Injury ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A ◽  
Deficient Mice

The role of natriuretic peptide receptor-A signaling in unilateral lung ischemia-reperfusion injury in the intact mouse

2008 ◽  
Vol 294 (4) ◽  
pp. L714-L723 ◽  
Author(s):  
Jeffrey M. Dodd-o ◽  
Maria L. Hristopoulos ◽  
Kathleen Kibler ◽  
Jolanta Gutkowska ◽  
Suhayla Mukaddam-Daher ◽  
...  
Keyword(s):  
Lung Injury ◽  
Natriuretic Peptide ◽  
Ischemia Reperfusion ◽  
Intracellular Camp ◽  
Natriuretic Peptide Receptor ◽  
Intact Mouse ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A

Ischemia-reperfusion (IR) causes human lung injury in association with the release of atrial and brain natriuretic peptides (ANP and BNP), but the role of ANP/BNP in IR lung injury is unknown. ANP and BNP bind to natriuretic peptide receptor-A (NPR-A) generating cGMP and to NPR-C, a clearance receptor that can decrease intracellular cAMP. To determine the role of NPR-A signaling in IR lung injury, we administered the NPR-A blocker anantin in an in vivo SWR mouse preparation of unilateral lung IR. With uninterrupted ventilation, the left pulmonary artery was occluded for 30 min and then reperfused for 60 or 150 min. Anantin administration decreased IR-induced Evans blue dye extravasation and wet weight in the reperfused left lung, suggesting an injurious role for NPR-A signaling in lung IR. In isolated mouse lungs, exogenous ANP (2.5 nM) added to the perfusate significantly increased the filtration coefficient sevenfold only if lungs were subjected to IR. This effect of ANP was also blocked by anantin. Unilateral in vivo IR increased endogenous plasma ANP, lung cGMP concentration, and lung protein kinase G (PKGI) activation. Anantin enhanced plasma ANP concentrations and attenuated the increase in cGMP and PKGI activation but had no effect on lung cAMP. These data suggest that lung IR triggered ANP release and altered endothelial signaling so that NPR-A activation caused increased pulmonary endothelial permeability.

scholarly journals Role of Natriuretic Peptide Receptor Guanylyl Cyclase-A in Myocardial Infarction Evaluated Using Genetically Engineered Mice

Hypertension ◽  
2005 ◽  
Vol 46 (2) ◽  
pp. 441-447 ◽  
Author(s):  
Michio Nakanishi ◽  
Yoshihiko Saito ◽  
Ichiro Kishimoto ◽  
Masaki Harada ◽  
Koichiro Kuwahara ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Genetically Engineered ◽  
Natriuretic Peptide Receptor ◽  
Peptide Receptor ◽  
Genetically Engineered Mice
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