Changes in the circadian rhythm of blood pressure in primary aldosteronism in response to dietary sodium restriction and adrenalectomy

1998 ◽  
Vol 16 (12) ◽  
pp. 1745-1748 ◽  
Author(s):  
Takashi Uzu ◽  
Masataka Nishimura ◽  
Takashi Fujii ◽  
Masanobu Takeji ◽  
Setsuko Kuroda ◽  
...  
2002 ◽  
Vol 25 (5) ◽  
pp. 737-742 ◽  
Author(s):  
Hiroshi TAKAKUWA ◽  
Kazuaki SHIMIZU ◽  
Yoshiaki IZUMIYA ◽  
Tamayo KATO ◽  
Izaya NAKAYA ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1502
Author(s):  
Katarzyna Łabno-Kirszniok ◽  
Agata Kujawa-Szewieczek ◽  
Andrzej Wiecek ◽  
Grzegorz Piecha

Increased marinobufagenin (MBG) synthesis has been suggested in response to high dietary salt intake. The aim of this study was to determine the effects of short-term changes in sodium intake on plasma MBG levels in patients with primary salt-sensitive and salt-insensitive hypertension. In total, 51 patients with primary hypertension were evaluated during acute sodium restriction and sodium loading. Plasma or serum concentrations of MBG, natriuretic pro-peptides, aldosterone, sodium, potassium, as well as hematocrit (Hct) value, plasma renin activity (PRA) and urinary sodium and potassium excretion were measured. Ambulatory blood pressure monitoring (ABPM) and echocardiography were performed at baseline. In salt-sensitive patients with primary hypertension plasma MBG correlated positively with diastolic blood pressure (ABPM) and serum NT-proANP concentration at baseline and with serum NT-proANP concentration after dietary sodium restriction. In this subgroup plasma MBG concentration decreased during sodium restriction, and a parallel increase of PRA was observed. Acute salt loading further decreased plasma MBG concentration in salt-sensitive subjects in contrast to salt insensitive patients. No correlation was found between plasma MBG concentration and left ventricular mass index. In conclusion, in salt-sensitive hypertensive patients plasma MBG concentration correlates with 24-h diastolic blood pressure and dietary sodium restriction reduces plasma MBG levels. Decreased MBG secretion in response to acute salt loading may play an important role in the pathogenesis of salt sensitivity.


2013 ◽  
Vol 46 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Lidiane Silva Rodrigues Telini ◽  
Gabriela de Carvalho Beduschi ◽  
Jacqueline Costa Teixeira Caramori ◽  
João Henrique Castro ◽  
Luis Cuadrado Martin ◽  
...  

1983 ◽  
Vol 245 (6) ◽  
pp. H1081-H1084 ◽  
Author(s):  
C. B. Toal ◽  
F. H. Leenen

Blood pressure and body weight of conscious spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were measured up to 16 wk of age in animals started at birth on five different sodium-containing diets. SHR on 9 mumol sodium/g food did not show a rise in basal blood pressure; however, when stressed the SHR still exhibited slightly higher blood pressures than WKY. In SHR on 17 mumol sodium/g food the development of hypertension was blunted compared with that of control (101 mumol/g) diet animals. SHR on 26 or 44 mumol sodium/g diet exhibited a development of hypertension similar to that of SHR on control diet. The 26 mumol/g, 44 mumol/g, and control sodium diet groups, regardless of strain, had similar growth rates. By contrast, on 17 mumol sodium/g food both SHR and WKY showed a substantially reduced growth rate, and all animals on 9 mumol sodium/g diet were severely retarded in growth. The results indicate that dietary sodium restriction can ameliorate the development of hypertension in SHR, but only when the sodium levels are so low as to affect overall growth.


2016 ◽  
Vol 101 (11) ◽  
pp. 3989-3996 ◽  
Author(s):  
Rene Baudrand ◽  
Francisco J. Guarda ◽  
Jasmine Torrey ◽  
Gordon Williams ◽  
Anand Vaidya

Context: The aldosterone to renin ratio (ARR) is recommended to screen for primary aldosteronism (PA). Objective: To evaluate whether dietary sodium restriction results in misinterpretation of PA screening. Participants: Untreated hypertensives with ARR more than 20 on a high dietary sodium intake (HS) were also evaluated on a low dietary sodium intake (LS) (n = 241). Positive screening for PA was defined as: plasma renin activity (PRA) less than or equal to 1.0 ng/mL · h with serum aldosterone more than or equal to 6 ng/dL. PA was confirmed by a 24-hour urinary aldosterone excretion more than or equal to 12 mcg with urinary sodium more than 200 mmol. Results: Only 33% (79/241) of participants with an ARR more than 20 had a positive PA screen on HS. On LS, 56% (44/79) of these participants no longer met criteria for positive PA screening. When compared with participants with positive PA screening on both diets, participants with a positive screen on HS but negative on LS exhibited a significantly higher PRA on both diets. Remarkably, of the 48/79 participants who had PA confirmed, 52% had negative PA screening on LS. The distinguishing feature of these participants with “discordant” screening results was a larger rise in PRA on LS resulting in normalization of the ARR and higher Caucasian race prevalence. Conclusions: Sodium restriction is recommended in hypertension; however, it can significantly raise PRA, normalize the ARR, and result in false interpretation of PA screening. Milder phenotypes of PA, where PRA is not as suppressed, are most susceptible to dietary sodium influences on renin and ARR. Optimal screening for PA should occur under conditions of HS.


1978 ◽  
Vol 45 (6) ◽  
pp. 870-874 ◽  
Author(s):  
F. H. Leenen ◽  
P. Boer ◽  
G. G. Geyskes

Changes in heart rate, blood pressure, and plasma renin activity (PRA) were assessed during infusion of increasing doses of isoproterenol and during increasing work loads of dynamic exercise in five normal young men. Studies were performed at three levels of dietary sodium restriction: normal, moderately, and more severely restricted. Isoproterenol induced the expected dose-related increases in heart rate, systolic blood pressure, and PRA and decreases in diastolic blood pressure. Changes in dietary sodium intake affected these changes only to a minor degree. Dynamic exercise also induced the expected work-load-related increases in heart rate, systolic blood pressure, and PRA and decreases in diastolic blood pressure. Also these changes were not significantly affected by changes in dietary sodium intake. Apparently dietary sodium restriction does not sensitize the renin-releasing mechanisms to sympathetic stimulation.


1998 ◽  
Vol 274 (3) ◽  
pp. E403-E409 ◽  
Author(s):  
Donald R. Dengel ◽  
Robert V. Hogikyan ◽  
Michael D. Brown ◽  
Scott G. Glickman ◽  
Mark A. Supiano

The purpose of this study was to determine whether sodium-resistant hypertensives are more insulin resistant and whether dietary sodium restriction improves insulin sensitivity in older hypertensives. Insulin sensitivity was assessed by a frequently sampled intravenous glucose tolerance test to determine the insulin sensitivity index (SI) after 1 wk each of low- (20 mmol ⋅ l−1 ⋅ day−1) and high- (200 mmol ⋅ l−1 ⋅ day−1) sodium diets in 21 older (63 ± 2 yr) hypertensives. Subjects were grouped on the difference in mean arterial blood pressure (MABP) between diets [sodium sensitive (SS): ≥5-mmHg increase in MABP on the high-sodium diet ( n = 14); sodium resistant (SR): <5-mmHg increase in MABP on the high-sodium diet ( n = 7)]. There was no dietary sodium effect on fasting plasma insulin or SI. An analysis of variance indicated a significant ( P = 0.0002) group effect, with SS individuals having lower fasting plasma insulins on the low- (13 ± 2 vs. 27 ± 3 μU/ml) and high- (12 ± 2 vs. 22 ± 3 μU/ml) sodium diets compared with SR individuals. Similarly, there was a significant ( P= 0.0002) group effect in regard to SI, with SS individuals having significantly higher SI on the low- (3.26 ± 0.60 vs. 0.91 ± 0.31 μU × 10−4 ⋅ min−1 ⋅ ml−1) and high- (3.45 ± 0.51 vs. 1.01 ± 0.30 μU × 10−4 ⋅ min−1 ⋅ ml−1) sodium diets compared with SR individuals. We conclude that SR individuals exhibit a greater degree of insulin resistance than SS individuals and that dietary sodium restriction fails to improve insulin sensitivity regardless of sodium sensitivity status.


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