Effects of Dietary Sodium on Circadian Rhythm and Physiological Responses of 18-Hydroxycorticosterone

1983 ◽  
Vol 64 (3) ◽  
pp. 295-301 ◽  
Author(s):  
James R. Sowers ◽  
Victor I. Martin ◽  
Frances W. J. Beck

1. The effects of dietary sodium intake on plasma 18-hydroxycorticosterone (18-OHB) responses to physiological stimuli and recumbent 24-h-plasma 18-OHB levels have been examined in nine normal male subjects. 2. Basal supine levels of 18-OHB during a 40 mmol of sodium intake period (62.5 ± 6.0 ng/dl) were considerably greater (P < 0.0001) than the levels during a 200 mmol of sodium intake period (9.8 ± 1.2 ng/dl). Further incremental and percentage changes of 18-OHB in response to graded dose infusions of angiotensin II and adrenocorticotropic hormone (ACTH) were greater during the 40 mmol of sodium intake period. 3. Although the mean 24 h levels of plasma 18-OHB during the 40 mmol of sodium intake period (43.9 ± 4.0 ng/dl) were greater (P < 0.001) than those during the 200 mmol of sodium intake period (9.4 ± 1.2 ng/dl), the circadian rhythm of 18-OHB secretion was similar under the two extremes of sodium intake. 4. Factors which increase angiotensin II levels, such as sodium restriction, isometric exercise and angiotensin infusion, selectively increase 18-OHB and aldosterone, suggesting that angiotensin II increases 18-OHB and aldosterone secretion, in part, by modulation of the 18-hydroxylation reaction involved in conversion of corticosterone into 18-OHB.

1980 ◽  
Vol 59 (s6) ◽  
pp. 133s-135s ◽  
Author(s):  
S. L. Swartz ◽  
G. H. Williams ◽  
N. K. Hollenberg ◽  
F. R. Crantz ◽  
L. Levine ◽  
...  

1. Because changes in the plasma concentration of angiotensin II and bradykinin appear inadequate to account completely for the hypotensive response to captopril, we measured changes in plasma prostaglandins in response to increasing doses of captopril in nine supine normal male subjects studied on both a high (200 mol/l) and low (10 mol/l) sodium intake. 2. On both the high and low sodium diets, captopril induced significant (P&lt;0.01) increments in the 13,14-dihydro-15-keto metabolite of the vasodilatory prostaglandin E2, which correlated significantly with the fall in blood pressure (P&lt;0.0001). 3. No significant changes were noted in the plasma levels of 6-keto-prostaglandins F1α or thromboxane B2, the stable products of prostacyclin and thromboxane A2 respectively.


The effect of haemorrhage on aldosterone secretion was studied in anaesthetized dogs with intact pituitary glands and kidneys subjected to the stress of adrenal vein cannulation. The following observations were made: Acute haemorrhage was followed by a significant rise in aldosterone secretion in about one half of the animals studied. In most of the remaining dogs, called non-reactors, premature stimulation of aldosterone secretion before the withdrawal of blood appeared to be the cause for the lack of response. This stimulation was traced in many instances to prolonged surgical ‘stress’, in others to incipient circulatory failure. Another reason for a high initial secretion rate of aldosterone was low dietary sodium intake continued for a week or more. Increase in aldosterone secretion after haemorrhage was unimpaired by sectioning the vagi or the splanchnic nerves, and by the absence of the proprioceptors of carotid sinus and thyro-carotid junction, or of liver, spleen and gastrointestinal tract. During haemorrhage there is secretion of medullary amines and anoxia develops. The effect of these factors on aldosterone secretion was tested by infusing adrenaline and noradrenaline in the splanchnotomized animal, and by carrying out exchange transfusions with plasma till the dog had lost 50 % of its red cells. Provided the initial aldosterone secretion was low enough, these procedures caused small rises in output of aldosterone, but constituted less effective stimuli than blood loss. Glucocorticoid secretion was in all animals maximal or near maximal and changed but little in the course of the experiments. The findings suggest that, in the intact dog, aldosterone secretion is influenced by a variety of factors, most of which act indirectly by releasing ACTH , or renin, or both. The role of ACTH and of renin as mediators of the action of haemorrhage on secretion of aldosterone will be studied in part II.


2015 ◽  
Vol 113 (3) ◽  
pp. 488-497 ◽  
Author(s):  
Willem De Keyzer ◽  
Marcela Dofková ◽  
Inger Therese L. Lillegaard ◽  
Mieke De Maeyer ◽  
Lene Frost Andersen ◽  
...  

High dietary Na intake is associated with multiple health risks, making accurate assessment of population dietary Na intake critical. In the present study, reporting accuracy of dietary Na intake was evaluated by 24 h urinary Na excretion using the EPIC-Soft 24 h dietary recall (24-HDR). Participants from a subsample of the European Food Consumption Validation study (n 365; countries: Belgium, Norway and Czech Republic), aged 45–65 years, completed two 24 h urine collections and two 24-HDR. Reporting accuracy was calculated as the ratio of reported Na intake to that estimated from the urinary biomarker. A questionnaire on salt use was completed in order to assess the discretionary use of table and cooking salt. The reporting accuracy of dietary Na intake was assessed using two scenarios: (1) a salt adjustment procedure using data from the salt questionnaire; (2) without salt adjustment. Overall, reporting accuracy improved when data from the salt questionnaire were included. The mean reporting accuracy was 0·67 (95 % CI 0·62, 0·72), 0·73 (95 % CI 0·68, 0·79) and 0·79 (95 % CI 0·74, 0·85) for Belgium, Norway and Czech Republic, respectively. Reporting accuracy decreased with increasing BMI among male subjects in all the three countries. For women from Belgium and Norway, reporting accuracy was highest among those classified as obese (BMI ≥ 30 kg/m2: 0·73, 95 % CI 0·67, 0·81 and 0·81, 95 % CI 0·77, 0·86, respectively). The findings from the present study showed considerable underestimation of dietary Na intake assessed using two 24-HDR. The questionnaire-based salt adjustment procedure improved reporting accuracy by 7–13 %. Further development of both the questionnaire and EPIC-Soft databases (e.g. inclusion of a facet to describe salt content) is necessary to estimate population dietary Na intakes accurately.


1981 ◽  
Vol 61 (s7) ◽  
pp. 273s-275s ◽  
Author(s):  
W. Oelkers ◽  
A. Köhler ◽  
L. Belkien ◽  
R. Fuchs-Hammoser ◽  
M. Maiga ◽  
...  

1. Adrenocorticotropic hormone (ACTH; 10 i.u./day) was infused for 34 h into normal male subjects. Some subjects were additionally treated with propranolol or indomethacin. Others received sham infusions or hydrocortisone infusions instead of ACTH. 2. ACTH, but not sham or hydrocortisone infusions, led to a significant increase in plasma renin activity and angiotensin II concentration with a lag period of 7–10 h and a maximum response after 24 h. ACTH may be a physiological regulator of renin secretion, perhaps through a ‘trophic’ effect on the juxtaglomerular apparatus. 3. The effect of ACTH on renin is not mediated by a rise in plasma renin substrate, probably not by renal β-adrenoreceptors, but perhaps by prostaglandins. 4. A dissociation between plasma cortisol and aldosterone during ACTH infusion suggests that ACTH, in this dosage, stimulates aldosterone on the second day through renin and angiotensin II, before its secretion is finally suppressed during more prolonged infusion.


1979 ◽  
Vol 57 (3) ◽  
pp. 225-231 ◽  
Author(s):  
D. Gordon ◽  
W. S. Peart

1. The aim of this study was to test whether a postulated gastrointestinal or portal monitor of sodium intake plays any part in adjusting renal sodium excretion when dietary sodium is reduced. 2. Normal male subjects were given 50 mmol of sodium chloride intravenously three times daily for 3 days to replace or to supplement a constant oral intake of sodium chloride. 3. When oral sodium chloride was replaced with intravenous sodium chloride, renal sodium excretion remained constant. 4. When oral sodium chloride was kept constant, sodium administered as intravenous sodium chloride was promptly excreted in three out of four subjects. There was a delay in the increase in sodium excretion in the fourth subject. 5. Infusions containing 50 mmol of sodium chloride in 50 ml given intravenously over 22 min produced a rise in plasma sodium concentration and a fall in concentration of total plasma solids. 6. These results provide no evidence for a gastrointestinal or portal monitor of sodium intake, but do not disprove the existence of such a monitor.


1972 ◽  
Vol 70 (3) ◽  
pp. 533-551 ◽  
Author(s):  
J. Solc ◽  
D. Knorr

ABSTRACT Tetrahydroaldosterone-(THAldo)-glucuronide is the most important metabolite of aldosterone in the urine. According to Nicolis & Gabrilove (1969) we developed a GLC method for the determination of THAldo. The method includes the following steps: Enzymatic hydrolysis, extraction with ethylacetate, formation of γ-lactone, first TLC, formation of heptafluorobutyrate (HFB), second TLC, gas liquid chromatography (GLC) with electron capture detector (ECD), correction for losses by the internal 3H-THAldo standard. As little as 3 ng/sample can be detected with a coefficient of variation of < 10%. The paper presents more than 300 THAldo determinations during infancy and childhood. At the age of 5–30 days there is a significant (P < 0.01) peak of the THAldo excretion. The biological meaning of these high THAldo values in the early days of life is not clear at the present time. The peak is independent of the nutrition. After the age of 12 months the mean THAldo excretion is about 30 μg/m2/d. There is a circadian rhythm with a peak in the late morning. The dependence of the THAldo excretion on the sodium intake in childhood is the same as in adults. After potassium loading there is likewise a strong increase in the THAldo excretion. In a child suffering from Addison's disease we found about 30% of the substituted aldosterone as THAldo-glucuronide in the urine. As well angiotensin as ACTH induce an increase of the THAldo excretion. After dexamethasone there is a decrease of THAldo excretion indicating again an ACTH dependence of the aldosterone secretion. Children suffering from nephrotic syndrome during the active phase of the disease show very high values of THAldo in the urine. Under treatment with corticosteroids the THAldo excretion decreases depending on the remission. Treatment with both furosemide and potassium induces again a sharp increase of the THAldo excretion.


1992 ◽  
Vol 82 (4) ◽  
pp. 397-405 ◽  
Author(s):  
Joseph G. Motwani ◽  
Allan D. Struthers

1. The response of systemic and regional haemodynamic indices to increasing infusion rates of angiotensin II (1, 3 or 10 ng min−1 kg−1) or placebo [5% (w/v) d-glucose] was studied in eight normal male subjects. 2. As compared with placebo, angiotensin II infusion caused an incremental rise in the serum angiotensin II level [14.5 ± 7.7 (placebo) to 187.2 ± 36.1 (10 ng of angiotensin II min−1 kg−1) pmol/l; mean ± 95% confidence interval] associated with a stepwise increase in total peripheral resistance [880 ± 42 (placebo) to 1284 ± 58 (10 ng of angiotensin II min−1 kg−1) dyn s cm−5] and a progressive reduction in cardiac output [8.3 ± 0.4 (placebo) to 7.0 ± 0.4 (10 ng of angiotensin II min−1 kg−1) litres/min]. 3. A stepwise fall in renal blood flow was observed with increasing angiotensin II infusion rate [1302 ± 65 (placebo) to 913 ± 64 (10 ng of angiotensin II min−1 kg−1) ml/min]. In contrast, calf blood flow was unaffected by 1 ng or 3 ng of angiotensin II min−1 kg−1 and was significantly increased by 10 ng of angiotensin II min−1 kg−1 (P < 0.01). 4. Calf venous capacitance was uninfluenced by 1 ng of angiotensin II min−1 kg−1, but was significantly increased by both 3 ng (P < 0.005) and 10 ng (P < 0.001) of angiotensin II min−1 kg−1. 5. Our results indicate that the pressor response to angiotensin II is a summation of multiple regional haemodynamic effects which differ qualitatively not only with the vascular bed studied but also within a single tissue, with the level of circulating angiotensin II attained. 6. The venodilatation we have demonstrated with high angiotensin II levels may effect a potentially favourable redistribution of blood flow in situations of inappropriate extracellular fluid volume expansion, such as chronic heart failure.


1987 ◽  
Vol 113 (1) ◽  
pp. 139-146 ◽  
Author(s):  
J. M. C. Connell ◽  
G. Tonolo ◽  
D. L. Davies ◽  
J. Finlayson ◽  
S. G. Ball ◽  
...  

ABSTRACT Infusion of dopamine is reported to reduce the response of aldosterone to infused angiotensin II in sodium-deplete but not sodium-replete man. Six normal male subjects were infused with angiotensin II in graded doses (2, 4 and 8 ng/kg per min) with or without dopamine (1·0 μg/kg per min) during both dietary sodium repletion and depletion. The responses of both aldosterone and 18-hydroxycorticosterone to infusion of angiotensin II appeared to be reduced by dopamine in sodium-deplete, but not sodium-replete, subjects. However, when the relationships between plasma concentrations of angiotensin II and corticosteroid were examined it was evident that plasma concentrations of angiotensin II were lower when dopamine was infused concurrently with the peptide (P<0·05). In a second study, six sodium-deplete males were infused with angiotensin II at a constant rate (6 ng/kg per min) while dopamine (or placebo) was given in graded doses (0·5,1 and 5 μg/kg per min). Renal plasma flow was estimated from total body clearance of para-aminohippuric acid. Overall, angiotensin II concentrations were lower during dopamine infusion compared with those during infusion of placebo (63·2 ± 9·7 (s.e.m.) vs 92·3±6·4 pmol/l; P<0·01) and this was associated with a 40% increase in effective renal plasma flow (627 ± 68 vs 451 ± 15 ml/min; P < 0·05); there again appeared to be a reduced aldosterone response during combined angiotensin II/dopamine infusion compared with that during infusion of angiotensin II alone (1003 ± 404 vs 1225± 146 pmol/l; 0·05<P<0·1). Dopamine appeared to increase the metabolic clearance of infused angiotensin II, possibly by altering blood flow through vascular beds, such as renal, which degrade the peptide. This may partly explain the effects of dopamine on the response of the adrenal to infusion of angiotensin II in sodium-deplete man; the physiological role of dopamine in the regulation of corticosteroidogenesis remains speculative. J. Endocr. (1987) 113, 139–146


2004 ◽  
Vol 5 (4) ◽  
pp. 169-175 ◽  
Author(s):  
Enzo R Porrello ◽  
Catherine E Huggins ◽  
Claire L Curl ◽  
Andrea A Domenighetti ◽  
Thierry Pedrazzini ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Karim Parastouei ◽  
Mojtaba Sepandi ◽  
Eslam Eskandari

Abstract Background Epidemiological studies indicate increased prevalence of cardiovascular disease (CVD) among military personnel. Accordingly, identification of at-risk individuals and lifestyle modification such as improving diet quality can potentially inhibits the increasing trend of CVD mortality. The aim of this study was predicting the 10-year risk of CVD and its association with healthy diet indicator (HDI) among military personnel. Methods In this cross-sectional study, 400 male military personnel within the age range of 30–75 years were included. HDI score was calculated based on food frequency questionnaire, and the 10-year risk of CVD was evaluated using Framingham risk score (FRS). The FRS items include age, gender, total cholesterol, high density lipoprotein cholesterol (HDL-C), systolic blood pressure, status of diabetes and smoking. Partial correlation test was employed to investigate the relationship between Framingham risk score and HDI score. Results The mean age and body mass index (BMI) of participants were 38.67 ± 5.3 year and 25.28 ± 3.22 kg/m2, respectively. Prediction of FRS was as follows: 96.5% were low risk, 2% were moderate risk, and 1.5% were high risk. The mean HDI score of participants in this study was 5.98 ± 1.36. While HDI score did not show a significant correlation with FRS (r: − 0.009, p:0.860), increased dietary sodium intake had a significant positive correlation with FRS (r: 0.114, p:0.026). Conclusion The most of participants (96.5%) had in low risk of CVD development in the next 10 years. Meanwhile, the FRS showed no significant relationship with HDI score. Further researches are required to confirm the results of the present study.


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