Effects of Aging on the Glomerular Capillaries, Blood Pressure, and Renal Function in Rats

2015 ◽  
pp. 157-162 ◽  
Author(s):  
Hans-Joachim Schurek ◽  
Janusz Panzer ◽  
Andreas Wiemeyer ◽  
Karlwilhelm K�hn ◽  
Bernhard Aeikens ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Effects Of Aging ◽  
Glomerular Capillaries

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.

scholarly journals Clinical response scores to predict blood pressure and renal function improvement following renal artery stenting for atherosclerotic renal artery stenosis

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Kablak-Ziembicka ◽  
A Roslawiecka ◽  
R Badacz ◽  
A Sokolowski ◽  
P Musialek ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Logistic Regression ◽  
Renal Function ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Predictive Models ◽  
Artery Stenosis ◽  
Atherosclerotic Renal Artery Stenosis ◽  
Baseline Serum ◽  
Kidney Length

Abstract Background It is little known about predictors of systolic (SBP) and diastolic (DBP) blood pressure or renal function (eGFR) improvement in patients with atherosclerotic renal artery stenosis (ARAS) undergoing stent-assisted angioplasty (PTA). Therefore, we aimed to build a prediction scores that would indicate characteristics of patient subsets with ARAS most likely to have clinical improvement following PTA. Methods 201 patients who underwent PTA for ARAS (2003–2018) were categorized as eGFR or SBP/DBP responders based on eGFR increase of ≥11 ml/min/1.73m2, decrease of SBP ≥20mmHg and DBP ≥5mmHg at 12-months following PTA. The remaining patients were classified as non-responders. The performance of logistic regression models were evaluated by basic decision characteristics. Continuous data have been transformed into binary coding with help of operating characteristic (ROC) curve. Predictive models have been constructed for each followed by construction of predictive models in each of 3 categories. Results Logistic regression analysis showed that: baseline SBP&gt;145 mmHg, DBP &gt;82 mmHg, previous myocardial infarction and Renal-Aotric-Ratio &gt;5.1 were independent influencing factors of SBP response, with relative risk percentage shares of 69.8%; 12.1%; 10.9%; and 7.2%, respectively (sensitivity: 82%, specificity: 86.3%, positive (PPV):82% and negative (NPV) predictive values: 86.3%). The DBP decrease prediction model included baseline SBP &gt;145 mmHg and DBP &gt;82 mmHg, the ARAS progression, index kidney length &gt;106 mm, and bilateral PTA with respective shares of 35.0%; 21.8%; 18.2%; 13.3% and 11.8%. (sensitivity: 76%, specificity: 77.8%, PPV: 80.7% and NPV: 72.6%). The eGFR increase was associated with baseline serum creatinine &gt;122 μmol/L but eGFR greater than 30 ml/min/1.73m2, index kidney length &gt;98 mm, end-diastolic velocity in index renal artery, renal resistive index &lt;0.74, and requirement for &gt;3 BP medications, with respective shares of 24.4%; 24.4%; 21.2%; 15% and 15% (sensitivity: 33.3%, specificity: 93.5%, PPV: 65.6% and NPV: 78.9%). Conclusions Current study identified clinical characteristics of patients who most likely to respond to PTA for ARAS. The sutability of the score should be verified in a prospective cohort of patients referred to PTA of ARAS Funding Acknowledgement Type of funding source: None

Effects of NG-nitro-L-arginine methyl ester on renal function and blood pressure

1991 ◽  
Vol 261 (6) ◽  
pp. F1033-F1037 ◽  
Author(s):  
V. Lahera ◽  
M. G. Salom ◽  
F. Miranda-Guardiola ◽  
S. Moncada ◽  
J. C. Romero
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Renal Function ◽  
Methyl Ester ◽  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Systemic Blood Pressure ◽  
Synthesis Inhibitor ◽  
Renal Changes ◽  
Dose Dependent

The dose-dependent effects of intravenous infusions of nitric oxide (NO) synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 0.1, 1, 10, and 50 micrograms.kg-1.min-1), were studied in anesthetized rats to determine whether the inhibitory actions of L-NAME are manifested primarily in alterations of renal function or whether they are the consequences of the increase in systemic blood pressure. Mean arterial pressure (MAP) was not altered by the intravenous L-NAME infusions of 0.1 and 1.0 microgram.kg-1.min-1. However, 0.1 microgram.kg-1.min-1 L-NAME induced a 30% decrease in urine flow rate (UV). The administration of 1.0 microgram.kg-1.min-1 L-NAME, in addition to decreasing UV, also decreased urinary sodium excretion (UNaV) and renal plasma flow (RPF). The intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 produced significant increases in MAP that reversed the initial fall in UV and UNaV, despite decreasing RPF and glomerular filtration rate (GFR). The administration of L-arginine alone (10 micrograms.kg-1.min-1) did not modify any of the parameters measured, but it effectively prevented all the hemodynamic and renal changes induced by the infusion of 50 micrograms.kg-1.min-1 L-NAME. These results suggest that the decrease in nitric oxide production induced by the intravenous infusion of L-NAME affects renal excretion of sodium and water in the absence of any significant change in blood pressure. At larger doses, L-NAME also produces hypertension that overrides the initial antinatriuretic effect.

Sign in / Sign up

Export Citation Format

Share Document