Dietary salt decreases cytosolic calcium in platelets from Dahl salt-sensitive rats

1995 ◽  
Vol 269 (5) ◽  
pp. R1225-R1229 ◽  
Author(s):  
T. Ishida ◽  
M. Ishida ◽  
H. Matsuura ◽  
R. Ozono ◽  
G. Kajiyama ◽  
...  

To determine whether abnormal cellular Ca2+ handling is involved in salt-induced hypertension of Dahl salt-sensitive rats (DS), we investigated Ca2+ handling in fura 2-loaded platelets of DS and Dahl salt-resistant rats (DR) fed a high-NaCl (8%) or a low-NacL (0.3%) diet for 4 wk from 5 wk of age. At 5 wk of age, blood pressure, resting cytosolic Ca2+ concentration ([Ca2+]i), the thrombin-evoked increase in [Ca2+]i and the size of internal Ca2+ stores of DS were comparable with those of DR. After 4 wk on the diets, resting [Ca2+]i of DS on high-NaCl diet was lower than that of DS on low-NaCl diet, and there was no effect of high salt intake on resting [Ca2+]i in DR. In DS, high salt intake attenuated the [Ca2+]i response to thrombin in the presence of external Ca2+. In contrast, the [Ca2+]i response to thrombin in the absence of external Ca2+ was enhanced by high salt intake in DS. The size of internal Ca2+ stores was increased by high salt intake in DS but not in DR. These data suggest that it is not obligatory for hypertension to be accompanied by an increase in platelet [Ca2+]i.

2005 ◽  
Vol 85 (2) ◽  
pp. 679-715 ◽  
Author(s):  
Pierre Meneton ◽  
Xavier Jeunemaitre ◽  
Hugh E. de Wardener ◽  
Graham A. Macgregor

Epidemiological, migration, intervention, and genetic studies in humans and animals provide very strong evidence of a causal link between high salt intake and high blood pressure. The mechanisms by which dietary salt increases arterial pressure are not fully understood, but they seem related to the inability of the kidneys to excrete large amounts of salt. From an evolutionary viewpoint, the human species is adapted to ingest and excrete <1 g of salt per day, at least 10 times less than the average values currently observed in industrialized and urbanized countries. Independent of the rise in blood pressure, dietary salt also increases cardiac left ventricular mass, arterial thickness and stiffness, the incidence of strokes, and the severity of cardiac failure. Thus chronic exposure to a high-salt diet appears to be a major factor involved in the frequent occurrence of hypertension and cardiovascular diseases in human populations.


1993 ◽  
Vol 264 (6) ◽  
pp. H1810-H1816 ◽  
Author(s):  
M. A. Boegehold

This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4–5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.


2011 ◽  
Vol 110 (2) ◽  
pp. 468-471 ◽  
Author(s):  
Mirian J. Starmans-Kool ◽  
Alice V. Stanton ◽  
Yun Y. Xu ◽  
Simon A. McG Thom ◽  
Kim H. Parker ◽  
...  

Dietary salt intake is associated with high brachial blood pressure (BP) and increased risk of cardiovascular disease. We investigated whether changes in dietary salt intake are associated with changes in central BP and wave reflection in healthy volunteers. Ten healthy normotensive male volunteers (22–40 yr) participated in a 6-wk double-blind randomized crossover study to compare a low-dietary salt intake (60–80 mmol sodium/day) with a high-salt intake (low salt intake supplemented with 128 mmol sodium/day) on central BP and wave reflection. Brachial and carotid BP, carotid blood flow velocity, forward (Pf) and backward (Pb) pressure, wave intensity, body weight, and urinary electrolyte excretion were measured at the end of each crossover period. High salt intake significantly increased carotid systolic BP [98 (SD 11) vs. 91 mmHg (SD 13), P < 0.01] and increased wave reflection [ratio of backward to forward pressure (Pb/Pf) 0.13 (SD 0.02) vs. 0.11 (SD 0.03), P = 0.04] despite only small effects on brachial BP [114 (SD 9) vs. 112 mmHg (SD 6), P = 0.1]. Urinary sodium excretion and body weight were also increased following high salt intake. High salt intake disproportionately increases central BP compared with brachial BP as a result of enhanced wave reflection. These effects may contribute to the adverse effect of high dietary salt intake on the risk of cardiovascular disease.


2019 ◽  
Vol 2 (1) ◽  
pp. 14-18
Author(s):  
A O Adeagbo ◽  
O E Omosanya ◽  
A O Ayodapo ◽  
O T Elegbede ◽  
O M Shabi

As the prevalence of hypertension increases in adult Nigerians, achieving target blood pressure (BP) control has become an important management challenge. High salt intake is an important risk factor for hypertension and its high intake prevents adequate BP control. This study aims to explore the knowledge of salt intake and blood pressure control among hypertensive patients. Data were collected from a cross-sectional sample involving 564 adult hypertensive patients that were followed for at least 3 months prior to recruitment to this study. Data collection comprised interviewer-administered structured questionnaires about demographics, knowledge and practices related to salt, followed by measurement of blood pressure. A majority (92.9%) of the respondents knew that eating too much salt could affect health and less than one-half (40.1%) actually knew that not more than one teaspoon of salt should be consumed daily. Nearly all respondents (516) knew high BP to be a possible consequence of high salt intake. Among those that took a lot of salty food, 87.7% and 78.5% had high systolic BP and diastolic BP respectively. Although the majority of respondents were knowledgeable about the adverse effects of salt, few knew the daily intake recommended value. The higher the dietary salt intake, the higher the chances of having poor BP control. Increased knowledge about recommended salt intake and individual guidance could be important for reducing salt intake in hypertensive patients.


Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Keyona N King-Medina ◽  
Emily Henson ◽  
Pablo Ortiz

Human consumption of fructose as a sweetener has increased in the past 30 years. High fructose intake has been implicated in the development of hypertension, diabetes, and obesity. In the US, the upper 10th percentile of the population consumes up to 40% of their caloric intake from added sugars, in which fructose represents half of these. Fructose metabolism is strikingly different from that of glucose. Yet, the effect of a fructose or glucose-enriched diet in salt handling by the kidney, affecting blood pressure, and its interaction with high salt intake has been poorly studied. In genetic models of salt-sensitive hypertension, the activity of the Na + /K + /2Cl - cotransporter (NKCC2) in the thick ascending limb (TAL) is abnormally enhanced. We hypothesized that chronic fructose in drinking water induces a salt-dependent increase in blood pressure and stimulates NKCC2 during high salt intake in normal rats. Sprague-Dawley rats were given 20% fructose or 20% glucose in drinking water for 1 week after which a high salt (HS) diet (4% Na + in chow) was started for 3 weeks. When we measured systolic blood pressure (SBP) by tail cuff plethysmography in fructose-fed and glucose-fed rats on a HS diet, only the fructose-fed rats had an increased SBP from 120±10 to 132±6 mmHg on day 7 of HS (p<0.01). SBP continued to increase up to 144±18 mmHg after 3 weeks (p<0.01 vs glucose). Fructose or glucose alone did not increase SBP after 4 weeks. We then repeated the protocol using radiotelemetry to monitor the blood pressure (BP). In rats fed fructose, by day 5 of HS the SBP increased by 12±3 mmHg (p<0.02) and SBP remained elevated for 3 weeks (delta: 10±2.5 mmHg, n=3). In rats fed glucose, a HS diet did not significantly change SBP for 3 weeks (n=5). Moreover, NKCC2 activity in the TAL is enhanced by phosphorylation at Thr96, 101. We found that NKCC2 phosphorylation was higher in rats fed fructose plus HS (p<0.02) but not in rats fed glucose plus HS for 3 weeks (HS: 100, fructose+HS: 250±40%, glucose+HS: 95±10%). Therefore, we conclude that a high fructose (but not a glucose) diet in normal rats induces a salt-dependent increase in BP independently from caloric intake. Thus, the increase in BP may in part be due to the stimulation of NKCC2 phosphorylation in the TAL by fructose.


Author(s):  
Christine Y Bakhoum ◽  
Cheryl A M Anderson ◽  
Stephen P Juraschek ◽  
Casey M Rebholz ◽  
Lawrence J Appel ◽  
...  

Abstract BACKGROUND Uromodulin modulates the sodium-potassium-two-chloride transporter in the thick ascending limb of the loop of Henle, and its overexpression in murine models leads to salt-induced hypertension. We hypothesized that individuals with higher baseline levels of urine uromodulin would have a greater increase in systolic blood pressure (SBP) for the same increase in sodium compared with those with lower uromodulin levels. METHODS We used data from 157 subjects randomized to the control diet of the Dietary Approaches to Stop Hypertension (DASH)-Sodium trial who were assigned to 30 days of low (1,500 mg/d), medium (2,400 mg/d), and high salt (3,300 mg/d) diets in random order. Blood pressure was measured prerandomization and then weekly during each feeding period. We evaluated the association of prerandomization urine uromodulin with change in SBP between diets, as measured at the end of each feeding period, using multivariable linear regression. RESULTS Baseline urine uromodulin stratified by tertiles was ≤17.64, 17.65–31.97, and ≥31.98 µg/ml. Across the tertiles, there were no significant differences in SBP at baseline, nor was there a differential effect of sodium diet on SBP across tertiles (low to high, P = 0.81). After adjusting for age, sex, body mass index, and race, uromodulin levels were not significantly associated with SBP change from low to high sodium diet (P = 0.42). CONCLUSIONS In a randomized trial of different levels of salt intake, higher urine uromodulin levels were not associated with a greater increase in blood pressure in response to high salt intake.


2020 ◽  
Vol 33 (4) ◽  
pp. 371-371
Author(s):  
Hong-yi Wang ◽  
Yong-jie He ◽  
Wei Li ◽  
Fan Yang ◽  
Ning-ling Sun

Abstract Background To survey the relationship between salt intake and blood pressure in hypertensive patients in Beijing. Methods A cross-sectional survey was used. Essential hypertensive patients were enrolled and divided into three groups (low, medium, and high salt intake) according to their 24 h urinary sodium excretion, which was used to access the salt intake. Blood pressure was measured through office measurement and ambulatory blood pressure monitoring. Results A total of 2,241 patients were enrolled with a mean age of 59.5 ± 13.8 years, mean blood pressure of 141.1 ± 18.5/84.6 ± 12.7 mm Hg, and urinary sodium excretion of 163.9 (95% CI 160.3–167.4) mmol [equal to salt intake 9.59 (9.38–9.79) g/d]. There were 1,544 cases from tertiary hospitals and the other 697 cases from community hospitals. Patients from community hospitals took more salt than patients from tertiary hospitals. Patients with high salt intake were younger than patients with low and medium salt intake. There were more males in high salt intake group than in the other two groups. Ambulatory blood pressure monitoring showed that patients with high salt intake had higher mean blood pressure not only in daytime, but also at night. The diastolic blood pressure in patients with medium salt intake was higher than that in patients with low salt intake. Conclusions Higher salt intake was associated with higher ambulatory blood pressure in hypertensive patients. More effort should be made to lower salt intake to improve blood pressure control rate.


Author(s):  
Matthew C. Babcock ◽  
Austin T. Robinson ◽  
Kamila U. Migdal ◽  
Joseph C. Watso ◽  
Christopher R. Martens ◽  
...  

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