scholarly journals High-Salt Diet Enhances Vascular Reactivity in Pregnant Rats With Normal and Reduced Uterine Perfusion Pressure

Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 730-735 ◽  
Author(s):  
Laura A. Barron ◽  
Jena B. Giardina ◽  
Joey P. Granger ◽  
Raouf A. Khalil
Keyword(s):  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
High Salt ◽  
Pregnant Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
Uterine Perfusion

scholarly journals Low-Salt Diet Enhances Vascular Reactivity and Ca2+Entry in Pregnant Rats With Normal and Reduced Uterine Perfusion Pressure

Hypertension ◽  
2002 ◽  
Vol 39 (2) ◽  
pp. 368-374 ◽  
Author(s):  
Jena B. Giardina ◽  
Kathy L. Cockrell ◽  
Joey P. Granger ◽  
Raouf A. Khalil
Keyword(s):  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Pregnant Rats ◽  
Salt Diet ◽  
Low Salt ◽  
Uterine Perfusion

scholarly journals l-arginine Supplementation Increased Only Endothelium-Dependent Relaxation in Sprague-Dawley Rats Fed a High-Salt Diet by Enhancing Abdominal Aorta Endothelial Nitric Oxide Synthase Gene Expression

2020 ◽  
Vol 14 ◽  
pp. 117954682090284
Author(s):  
Abdullahi Adejare ◽  
Ahmed Oloyo ◽  
Chikodi Anigbogu ◽  
Smith Jaja
Keyword(s):  
Gene Expression ◽  
Vascular Reactivity ◽  
High Salt ◽  
Enos Gene ◽  
Sprague Dawley ◽  
High Salt Diet ◽  
Salt Diet ◽  
Sprague Dawley Rats ◽  
Endothelium Dependent Relaxation ◽  
Arginine Supplementation

Background: Abnormal vascular reactivity and reduced expression of endothelial nitric oxide synthase ( eNOS) gene are hallmark of salt-induced hypertension in rats. Although l-arginine is an established vasodilator, the mechanism by which it modulates vascular reactivity in salt-induced hypertension is not clearly understood. Objectives: This study was designed to investigate the mechanism by which oral l-arginine supplementation modulates vascular reactivity and eNOS gene expression in Sprague-Dawley rats fed a high-salt diet. Methods: Forty-eight weaned male Sprague-Dawley rats of weight range 90 to 110 g were randomly divided into 6 groups of 8 rats per group. Group I was fed normal rat chow ad libitum and served as the Normal Diet group. Group II was fed a diet that contained 8% NaCl. Groups III and IV took normal and high-salt diet, respectively, and then received oral l-arginine supplementation (100 mg/kg/day), while groups V and VI took normal and high-salt diet, respectively, and then were co-administered with both l-arginine and l-nitro-arginine methyl ester (L-NAME; 100 mg/kg/day and 40 mg/kg/day, respectively) orally. At the end of 12-week experimental period, the animals were sacrificed to assess vascular reactivity and gene expression level. Results: Our results show that high-salt diet significantly reduced ( P < .05) endothelium-dependent relaxation response to acetylcholine and qualitatively reduced eNOS gene expression in the abdominal aorta of the rats. However, l-arginine supplementation improved the impaired endothelium-dependent relaxation and nitric oxide level while ameliorating the reduced eNOS gene expressions. Conclusion: This study suggests that oral supplementation of l-arginine enhances endothelial-dependent relaxation in rats fed a high-salt diet by ameliorating eNOS gene expression in the abdominal aorta of the rats.

scholarly journals Effects of Testosterone on Vascular Reactivity in Male Sprague – Dawley Rats Fed a High Salt Diet

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Ahmed Kolade Oloyo ◽  
Yakubu Momoh ◽  
Olusoga Sofola ◽  
Adebayo Oyekan
Keyword(s):  
Vascular Reactivity ◽  
High Salt ◽  
Sprague Dawley ◽  
High Salt Diet ◽  
Salt Diet ◽  
Sprague Dawley Rats

scholarly journals Atrial natriuretic peptide and aldosterone secretions, and atrial natriuretic peptide-binding sites in kidneys and adrenal glands of pregnant and fetal rats in late gestation in response to a high-salt diet

2000 ◽  
pp. 524-532 ◽  
Author(s):  
S Deloof ◽  
C De Seze ◽  
V Montel ◽  
A Chatelain
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Adrenal Glands ◽  
Sodium Intake ◽  
High Salt ◽  
Pregnant Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Sodium ◽  
Fetal Rats

OBJECTIVE: This study aimed at determining, in the term pregnant rat, whether maternal and fetal plasma atrial natriuretic peptide (ANP) concentrations were modified in response to an oral sodium load, and to investigate whether any changes in plasma concentrations were able to modify the density and affinity of the different ANP-binding site subtypes in maternal and fetal kidneys and adrenal glands. METHODS: Pregnant rats kept in metabolic cages were divided into two groups. The normal sodium diet group had free access to rat chow and tap water whereas the high sodium diet group received 1% NaCl as drinking water for 10 consecutive days from day 11 to day 21 of gestation with free access to standard rat chow. Pregnant rats from both groups were killed by decapitation on day 21 of gestation. The plasma ANP and aldosterone concentrations were determined by RIA. The density and affinity of ANP receptors were determined in the maternal and fetal adrenal glands and kidneys. RESULTS: In the pregnant rats on the high-salt diet, the sodium and water intakes, as well as the urine volume and sodium excretion, were significantly higher than in the control group. After 10 days of high-salt intake, water and sodium retentions were not significantly different in the two groups, indicating that the pregnant rats were able to excrete excess salt. The high sodium intake did not change the body weight of the pregnant rats but did increase the body weight of the fetal rats. Maternal and fetal hematocrits remained unchanged in both groups, the high sodium intake did not modify plasma sodium concentration in the maternal rats but increased that of the fetuses, indicating an accumulation of sodium in the fetal rats. The dietary sodium intake did not change the plasma ANP concentrations but significantly decreased the plasma aldosterone concentrations in both the maternal and fetal rats. In response to the high-salt diet, the density and affinity of total ANP, ANPb and ANPc receptors were not altered in the maternal isolated renal glomeruli or the adrenal zona glomerulosa membranes or the fetal adrenal gland and kidney membrane preparations. CONCLUSION: These results suggest that ANP is not involved in the regulation of water and electrolyte balance in maternal and fetal rats during salt-loaded intake.

463-P: Deterioration of Atherosclerosis via Dysbiosis in ApoE Null Mice Fed with High-Salt Diet

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 463-P
Author(s):  
TOMONORI KIMURA ◽  
YOSHITAKA HASHIMOTO ◽  
TAKAFUMI SENMARU ◽  
EMI USHIGOME ◽  
MASAHIDE HAMAGUCHI ◽  
...  
Keyword(s):  
High Salt ◽  
High Salt Diet ◽  
Salt Diet

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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