scholarly journals Effect of intracerebroventricular epinephrine microinjection on blood pressure and urinary sodium handling in gestational protein-restricted male adult rat offspring

Biology Open ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. bio038562
Author(s):  
Bárbara Vaccari Cardoso ◽  
Augusto Henrique Custódio ◽  
Patrícia Aline Boer ◽  
José Antonio Rocha Gontijo
Keyword(s):  
Blood Pressure ◽  
Urinary Sodium ◽  
Male Adult ◽  
Adult Rat ◽  
Rat Offspring ◽  
Sodium Handling

[PP.30.05] BLOOD PRESSURE IN RELATION TO 24-HOUR URINARY SODIUM EXCRETION AND RENAL SODIUM HANDLING

2016 ◽  
Vol 34 ◽  
pp. e308
Author(s):  
K. Stolarz-Skrzypek ◽  
A. Bednarski ◽  
A. Franczyk ◽  
M. Folta ◽  
H. Barton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renal Sodium Handling ◽  
Sodium Handling

scholarly journals Gestational Protein Restriction Increases Cardiac Connexin 43 mRNA levels in male adult rat offspring

2017 ◽  
Author(s):  
Kamila Fernanda Rossini ◽  
Camila Andrea de Oliveira ◽  
Hércules Jonas Rebelato ◽  
Marcelo Augusto Marreto Esquisatto ◽  
Rosana Catisti
Keyword(s):  
Connexin 43 ◽  
Protein Restriction ◽  
Mrna Levels ◽  
Male Adult ◽  
Adult Rat ◽  
Rat Offspring

Influence of postnatal maternal stress on blood pressure and heart rate of juvenile and adult rat offspring

1990 ◽  
Vol 23 (8) ◽  
pp. 839-847 ◽  
Author(s):  
Elliott Mills ◽  
Joseph W. Bruckert ◽  
Peter G. Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Maternal Stress ◽  
Adult Rat ◽  
Rat Offspring

scholarly journals Effect of intracerebroventricular epinephrine microinjection on blood pressure and urinary sodium handling in gestational protein-restricted rat adult male offspring

2018 ◽  
Author(s):  
Bárbara Vaccari Cardoso ◽  
Augusto Henrique Custódio ◽  
Patrícia Aline Boer ◽  
José Antonio Rocha Gontijo
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Lateral Ventricle ◽  
Urinary Sodium Excretion ◽  
Good Evidence ◽  
Urinary Sodium ◽  
Adrenergic Agonists ◽  
Adrenoceptor Antagonist ◽  
Α2 Adrenoceptor ◽  
Sodium Handling

ABSTRACTBackgroundIn this study, we hypothesized that blunting of the natriuresis response to intracerebroventricularly (i.c.v.) microinjected adrenergic agonists are involved in the development of hypertension in maternal low-protein (LP) intake offspring. Methods. Stainless steel cannula was stereotaxically implanted into the right lateral ventricle, by use of techniques reported elsewhere and after that, was evaluated the effect of i.c.v. injection of adrenergic agonists, at increasing concentrations, and of α1 and α2-adrenoceptor antagonists on blood pressure and urinary sodium handling in LP offspring relative to age-matched, normal (NP) protein intake group.ResultsWe confirmed that epinephrine (Epi) microinjected into the lateral ventricle (LV) of conscious NP rats leads to enhanced natriuresis followed by a reduction in arterial pressure. This response was associated with increased proximal and post-proximal sodium excretion accompanied by an unchanged glomerular filtration rate. The current study showed in both, NP and LP offspring that natriuretic effect of Epi injection into the LV was abolished by prior local microinjection of an α1-adrenoceptor antagonist (prazosin). Conversely, LV α2-adrenoceptor antagonist (yohimbine) administration potentiated the action of epinephrine. The LV yohimbine pretreatment normalized urinary sodium excretion and reduced the blood pressure in LP compared with age-matched NP offspring.ConclusionThese are, as far as we are aware, the first results showing the role of central adrenergic receptors interaction on hypertension pathogenesis in maternal protein-restricted fetal programming offspring. The study also provides good evidence of the existence of central nervous system adrenergic mechanisms consisting of α1 and α2-adrenoceptors, which works reciprocally on the control of renal sodium excretion and blood pressure. Although the precise mechanism of the different natriuretic response of NP and LP rats is still uncertain, these results led us to speculate that inappropriate neural adrenergic pathways might have significant effects on tubule sodium transport, resulting in the inability of the kidneys to control hydrosaline balance, and, consequently, an increase in blood pressure.

scholarly journals Association between 24-h urinary sodium and potassium excretion and blood pressure among Chinese adults aged 18–69 years

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Inverse Association ◽  
Potassium Excretion ◽  
Chinese Adults ◽  
Potassium Intake ◽  
Sodium And Potassium

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.

scholarly journals Urinary sodium excretion and the risk of cardiovascular disease: A community-based cohort study in Taiwan

2021 ◽  
pp. 1-42
Author(s):  
Yi-Jie Wang ◽  
Kuo-Lioug Chien ◽  
Hsiu-Ching Hsu ◽  
Hung-Ju Lin ◽  
Ta-Chen Su ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Systolic Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Salt Sensitivity ◽  
Urinary Sodium ◽  
Mediating Effect ◽  
Cvd Risk ◽  
Media Thickness

Abstract Urinary sodium excretion is a potential risk factor for cardiovascular diseases (CVD). However, the underlying biological mechanisms and effects of salt sensitivity are unclear. The purpose of this study was to characterize the relative contribution of biological factors to the sodium-CVD association. A total of 2112 participants were enrolled in this study. Structured questionnaires and blood and urine samples were obtained. Twenty-four-hour sodium excretion was estimated using a single overnight urine sample. Hypertension, metabolic syndrome, and overweight status were considered to indicate salt sensitivity. Cox proportional hazard models were used to investigate the effects of salt sensitivity on urinary sodium excretion and CVD risk. The traditional mediation approach was used to calculate the proportion of mediation. The mean age (standard deviation) of the 2112 participants was 54.5 (12.2) years, and they were followed up for a mean of 14.1 [8.1] years. Compared with those in the lowest quartile, the highest baseline urinary sodium excretion (>4.2g/24 hours) was associated with a 43% higher CVD risk (hazard ratio, 1.43; 95% confidence interval, 1.02-1.99). Participants with high urinary sodium excretion, hypertension, or metabolic syndrome had a significantly high risk of CVD. The carotid intima-media thickness had the largest mediating effect (accounting for 35% of the sodium-CVD association), followed by systolic blood pressure (33%), left ventricular mass (28%), and diastolic blood pressure (14%). Higher urinary sodium excretion increased the risk of CVD, which was explained largely by carotid media-thickness and systolic blood pressure.

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