Renal Function and Blood Pressure: Molecular Insights into the Biology of Endothelin-1

2011 ◽  
pp. 18-34 ◽  
Author(s):  
Nicolas Vignon-Zellweger ◽  
Susi Heiden ◽  
Noriaki Emoto
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Endothelin 1

Plasma endothelin-1 level is related to renal function and smoking status but not to blood pressure

2004 ◽  
Vol 22 (4) ◽  
pp. 713-718 ◽  
Author(s):  
Yuji Hirai ◽  
Hisashi Adachi ◽  
Yoshihisa Fujiura ◽  
Akiko Hiratsuka ◽  
Mika Enomoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Smoking Status ◽  
Endothelin 1

1248: Impact of Surgical Treatment of Renal Carcinoma on Renal Function and Blood Pressure: A Race- and Age-Dependent Association

2007 ◽  
Vol 177 (4S) ◽  
pp. 411-412
Author(s):  
Javier Miller ◽  
Angela Smith ◽  
Kris Gunn ◽  
Erik Kouba ◽  
Eric M. Wallen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Surgical Treatment ◽  
Renal Carcinoma ◽  
Age Dependent

scholarly journals Association between polymorphism at IGF-1 rs35767 gene locus and long-term decline in renal function: a Japanese retrospective longitudinal cohort study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Kosuke Honda ◽  
Satoru Kuriyama ◽  
Kimiyoshi Ichida ◽  
Tomoko Nakano ◽  
Naoki Sugano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Renal Function ◽  
Uric Acid ◽  
Cohort Study ◽  
Serum Uric Acid Level ◽  
Human Growth ◽  
Longitudinal Cohort Study ◽  
Longitudinal Cohort

Abstract Background Insulin-like growth factor-1 (IGF-1) acts on glucose and protein metabolism and human growth and also influences blood pressure and renal function. This study investigated whether the single-nucleotide polymorphism of IGF-1, rs35767, plays a role in metabolic syndrome indicators, including blood pressure, glucose metabolism, uric acid levels, and renal function. Methods In this retrospective longitudinal cohort study, blood samples from 1506 Japanese individuals were collected and used for genotyping for variant rs35767: T > C in the IGF-1 upstream promoter. Data were analyzed to identify associations between IGF-1 genotypes and patient biochemical parameters, including the components of metabolic syndrome and the long-term change in renal function. Results The cohort rs35767 genotypes included 650 CC carriers (43.2%), 687 TC carriers (45.6%), and 169 TT carriers (11.2%). Multiple regression analysis revealed no association between IGF-1 genotype and blood pressure, glycated hemoglobin level, and serum uric acid level. However, in females, blood pressure was negatively correlated with the TT genotype. Longitudinal observation revealed that the decline in eGFR over 10 years was greater in TT (− 18.51 ± 1.04 mL/min/1.73m2) than in CC carriers (− 16.38 ± 0.52 mL/min/1.73m2; P < 0.05). Conclusion The present study suggests that renal function declines faster in individuals with the TT genotype at the IGF-1 rs35767 locus than in those with the CC genotype, suggesting that the TT genotype is associated with the long-term chronological decline in renal function.

scholarly journals Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

2019 ◽  
Vol 20 (14) ◽  
pp. 3495 ◽  
Author(s):  
Yanling Yan ◽  
Jiayan Wang ◽  
Muhammad A. Chaudhry ◽  
Ying Nie ◽  
Shuyan Sun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Significant Rise ◽  
Protein Carbonylation ◽  
High Salt ◽  
Kidney Cortex ◽  
High Salt Diet ◽  
Salt Diet ◽  
Salt Sensitive Hypertension

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

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