"IN VIVO RADIOIMMUNOASSAY" OF ALDOSTERONE

1973 ◽  
Vol 74 (2) ◽  
pp. 307-315 ◽  
Author(s):  
P. Vecsei ◽  
K. H. Gless ◽  
M. Winter ◽  
M. Hanka-Postozky

ABSTRACT Aldosterone antibodies were raised in sheep immunized with a complex of D-aldosterone-21-hemisuccinate and bovine serum albumin. The intravenous injection of these antibodies into rats caused a delay in the disappearance rate of tritiated aldosterone from the blood. The degree of this effect depends on the body weight of the animals, on the amount of the antiserum given, and on the interval between the injection of antibodies and that of labelled aldosterone. After the injection of aldosterone antibodies and the tritiated hormone, the plasma concentration of labelled aldosterone was related to the rate of secretion of the hormone. When aldosterone secretion was low, subsequent to high sodium intake, or abolished after adrenalectomy, the plasma concentration of tritiated aldosterone was higher than in the control rats. Stimulation of aldosterone secretion by furosemide or ACTH, or administration of cold aldosterone resulted in a decrease in the plasma concentration of the labelled hormone. It is suggested that the relationship between the amount of free aldosterone in the "inner pool" and the plasma concentration of tritiated aldosterone is the consequence of a competition of labelled and unlabelled hormone for the binding capacity of the antibody.

1987 ◽  
Vol 73 (1) ◽  
pp. 93-97 ◽  
Author(s):  
G. C. Inglis ◽  
C. J. Kenyon ◽  
J. A. M. Hannah ◽  
J. M. C. Connell ◽  
S. G. Ball

1. This study investigated the role of dopamine in the control of adrenal steroidogenesis. Adrenaline, noradrenaline and dopamine have been measured in plasma and in the adrenal zona glomerulosa and medulla of rats fed low, normal and high sodium diets and in zona glomerulosa tissue of rats with adrenal regeneration hypertension (ARH). 2. Adrenal concentrations (means ± se) of adrenaline, noradrenaline and dopamine in rats fed a normal diet were 1471 ± 335, 527 ± 75 and 51 ± 12 nmol/g in the medulla, and 66 ± 17, 18 ± 9 and 6 ± 1 nmol/g in the zona glomerulosa. The dopamine content of the zona glomerulosa was greater than could be accounted for by simple contamination from the medullary catecholamines and is commensurate with that of tissue with dopaminergic innervation. 3. Adrenal noradrenaline and adrenaline concentrations and plasma catecholamine and corticosterone concentrations were not affected by dietary sodium intake. Plasma aldosterone concentrations were > 3030.4, 339.8 ± 41.5 and 55.2 ± 11.0 pmol/l in rats fed low, normal and high sodium diets respectively. 4. Five weeks after right adrenalectomy and nephrectomy and left adrenal enucleation, ARH rat systolic blood pressure had increased by 47 mmHg. In the regenerated gland, the concentrations of noradrenaline and adrenaline were negligible but dopamine was present in amounts similar to that of a normal adrenal cortex. 5. Dopamine is present in the adrenal zona glomerulosa in significant amounts but does not decrease when dietary sodium intake is reduced and is not inversely related to aldosterone secretion. These observations are compatible with findings in vivo which indicate that dopamine inhibits aldosterone secretion by an extra-adrenal process involving increased clearance of the major aldosterone trophin angiotensin II.


2019 ◽  
Vol 56 (2) ◽  
pp. 65-76
Author(s):  
Shi-Cheng Li ◽  
Qing-Hai Wang ◽  
Lian-Feng Chen ◽  
Shu-Yi Feng ◽  
Yan-Xiang Wu ◽  
...  

1992 ◽  
Vol 70 (4) ◽  
pp. 580-586 ◽  
Author(s):  
Eef Harmsen ◽  
Frans H. H. Leenen

In humans, high sodium intake not only increases the blood pressure, and thus can cause left ventricular hypertrophy (LVH), but also appears to increase LVH independent of this increase in blood pressure. In both normo- and hyper-tensive rats the hypertrophic effect of increased dietary sodium intake on the heart has been clearly established. In normotensive rats, this effect is strain and age dependent, and seems independent of hemodynamic effects of high sodium intake. In both rats and humans, dietary sodium appears to increase wall thickness, resembling pressure overload rather than an increased left ventricular diameter as expected of volume overload. The mechanisms through which high dietary sodium induces hypertrophy are still unknown. It is possible that dietary sodium increases either adrenergic stimulation and (or) enhances sensitivity for adrenergic stimulation and that this hypertrophic response mainly acts via stimulation of α1-adrenergic receptors. Stimulation of the α1-adrenergic receptors will increase the inositol phosphate – diacyl glycerol pathway and enhance the Na+/H+ exchange. The activity of this exchanger might play an important role in the development of dietary sodium induced cardiac hypertrophy.Key words: heart, dietary sodium, left ventricular hypertrophy, hemodynamics, sympathetic activity.


2021 ◽  
Vol 40 (S1) ◽  
Author(s):  
Ruhaya Salleh ◽  
Shubash Shander Ganapathy ◽  
Norazizah Ibrahim Wong ◽  
Siew Man Cheong ◽  
Mohamad Hasnan Ahmad ◽  
...  

Abstract Background Studies have shown that having away from home meals contributes to high sodium intake among young people and those who lived in urban areas. This study aimed to determine the association between dietary sodium intake, body mass index, and away from home meal consumption behaviour among Malaysian adults. Methods MyCoSS was a cross-sectional household survey involving 1440 adults age 18 years and above. This study utilized stratified cluster sampling to obtain a nationally representative sample. Data was collected between October 2017 and March 2018. Socio-demographic information, dietary assessment using food frequency questionnaire (FFQ), and away from home meal consumption were assessed through a face-to-face interview by trained health personnel. Descriptive analysis and logistic regression were applied to identify the association of socioeconomic status and away from home meal consumption with dietary sodium intake. Results A total of 1032 participants completed the FFQ, with a mean age of 48.8 + 15.6 years. Based on the FFQ, slightly over half of the participants (52.1%) had high sodium intake. Results showed that 43.6% of participants consumed at least one to two away from home meals per day, while 20.8% of them had their three main meals away from home. Participants aged less than 30 years old were the strongest predictor to consume more sodium (adjusted OR: 3.83; 95%CI: 2.23, 6.58) while those of Indian ethnicity had significantly lower sodium intake. Surprisingly, having three away from home meals per day was not associated with high dietary sodium intake, although a significant association (crude OR; 1.67, 95% CI: 1.19, 2.35) was found in the simple logistic regression. Obese participants were less likely to have high dietary sodium intake compared with the normal BMI participants in the final model. Conclusion Over half of the participants consumed sodium more than the recommended daily intake, especially those who consumed three away from home meals. However, there was no significant association between high sodium intake and having three away from home meals per day. The promotion of healthy cooking methods among the public must continue to be emphasized to reduce the dietary sodium intake among Malaysian adults.


2012 ◽  
Vol 303 (3) ◽  
pp. F412-F419 ◽  
Author(s):  
Preethi Samuel ◽  
Quaisar Ali ◽  
Rifat Sabuhi ◽  
Yonnie Wu ◽  
Tahir Hussain

High sodium intake is known to regulate the renal renin-angiotensin system (RAS) and is a risk factor for the pathogenesis of obesity-related hypertension. The complex nature of the RAS reveals that its various components may have opposing effects on natriuresis and blood pressure regulation. We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT1R) vs. AT2-ACE2-angiotensinogen (Ang) (1–7)-Mas receptor (MasR), in obesity. In the present study, we evaluated protein and/or mRNA expression of angiotensinogen, renin, AT1A/BR, ACE, AT2R, ACE2, and MasR in the kidney cortex following 2 wk of a 8% high-sodium (HS) diet in lean and obese Zucker rats. The expression data showed that the relative expression pattern of ACE and AT1BR increased, renin decreased, and ACE2, AT2R, and MasR remained unaltered in HS-fed lean rats. On the other hand, HS intake in obese rats caused an increase in the cortical expression of ACE, a decrease in ACE2, AT2R, and MasR, and no changes in renin and AT1R. The cortical levels of ANG II increased by threefold in obese rats on HS compared with obese rats on normal salt (NS), which was not different than in lean rats. The HS intake elevated mean arterial pressure in obese rats (27 mmHg) more than in lean rats (16 mmHg). This study suggests that HS intake causes a pronounced increase in ANG II levels and a reduction in the expression of the ACE2-AT2R-MasR axis in the kidney cortex of obese rats. We conclude that such changes may lead to the potentially unopposed function of AT1R, with its various cellular and physiological roles, including the contribution to the pathogenesis of obesity-related hypertension.


2011 ◽  
Vol 301 (2) ◽  
pp. F334-F343 ◽  
Author(s):  
David W. Good ◽  
Thampi George ◽  
Bruns A. Watts

A high sodium intake increases the capacity of the medullary thick ascending limb (MTAL) to absorb HCO3−. Here, we examined the role of the apical NHE3 and basolateral NHE1 Na+/H+ exchangers in this adaptation. MTALs from rats drinking H2O or 0.28 M NaCl for 5–7 days were perfused in vitro. High sodium intake increased HCO3− absorption rate by 60%. The increased HCO3− absorptive capacity was mediated by an increase in apical NHE3 activity. Inhibiting basolateral NHE1 with bath amiloride eliminated 60% of the adaptive increase in HCO3− absorption. Thus the majority of the increase in NHE3 activity was dependent on NHE1. A high sodium intake increased basolateral Na+/H+ exchange activity by 89% in association with an increase in NHE1 expression. High sodium intake increased apical Na+/H+ exchange activity by 30% under conditions in which basolateral Na+/H+ exchange was inhibited but did not change NHE3 abundance. These results suggest that high sodium intake increases HCO3− absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. These studies support a role for NHE1 in the long-term regulation of renal tubule function and suggest that the regulatory interaction whereby NHE1 enhances the activity of NHE3 in the MTAL plays a role in the chronic regulation of HCO3− absorption. The adaptive increases in Na+/H+ exchange activity and HCO3− absorption in the MTAL may play a role in enabling the kidneys to regulate acid-base balance during changes in sodium and volume balance.


1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.


2017 ◽  
Vol 35 ◽  
pp. e89
Author(s):  
M. Rhee ◽  
J. Kim ◽  
S. Shin ◽  
D. Nah ◽  
N. Gu ◽  
...  

2007 ◽  
Vol 293 (4) ◽  
pp. R1657-R1665 ◽  
Author(s):  
Annie Beauséjour ◽  
Véronique Houde ◽  
Karine Bibeau ◽  
Rébecca Gaudet ◽  
Jean St-Louis ◽  
...  

Sodium supplementation given for 1 wk to nonpregnant rats induces changes that are adequate to maintain renal and circulatory homeostasis as well as arterial blood pressure. However, in pregnant rats, proteinuria, fetal growth restriction, and placental oxidative stress are observed. Moreover, the decrease in blood pressure and expansion of circulatory volume, normally associated with pregnancy, are prevented by high-sodium intake. We hypothesized that, in these pregnant rats, a loss of the balance between prooxidation and antioxidation, particularly in kidneys and heart, disturbs the normal course of pregnancy and leads to manifestations such as gestational hypertension. We thus investigated the presence of oxidative/nitrosative stress in heart and kidneys following high-sodium intake in pregnant rats. Markers of this stress [8-isoprostaglandin F2α (8-iso-PGF2α) and nitrotyrosine], producer of nitric oxide [nitric oxide synthases (NOSs)], and antioxidants [superoxide dismutase (SOD) and catalase] were measured. Then, molecules (Na+-K+-ATPase and aconitase) or process [apoptosis (Bax and Bcl-2), inflammation (monocyte chemoattractant protein-1, connective tissue growth factor, and TNF-α)] susceptible to free radicals was determined. In kidneys from pregnant rats on 1.8% NaCl-water, NOSs, apoptotic index, and nitrotyrosine expression were increased, whereas Na+-K+-ATPase mRNA and activity were decreased. In the left cardiac ventricle of these rats, heightened nitrotyrosine, 8-iso-PGF2α, and catalase activity together with reduced endothelial NOS protein expression and SOD and aconitase activities were observed. These findings suggest that oxidative/nitrosative stress in kidney and left cardiac ventricle destabilizes the normal course of pregnancy and could lead to gestational hypertension.


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