scholarly journals High Salt Intake Increases Blood Pressure in Normal Rats: Putative Role of 20-HETE and No Evidence on Changes in Renal Vascular Reactivity

2015 ◽  
Vol 40 (3) ◽  
pp. 323-334 ◽  
Author(s):  
A. Walkowska ◽  
M. Kuczeriszka ◽  
J. Sadowski ◽  
K.H. Olszyñski ◽  
L. Dobrowolski ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Reactivity ◽  
Salt Intake ◽  
High Salt ◽  
Putative Role ◽  
High Salt Intake ◽  
Renal Vascular

Blunted hypertensive effect of combined fructose and high-salt diet in gene-targeted mice lacking functional serum- and glucocorticoid-inducible kinase SGK1

2006 ◽  
Vol 290 (4) ◽  
pp. R935-R944 ◽  
Author(s):  
Dan Yang Huang ◽  
Krishna M. Boini ◽  
Björn Friedrich ◽  
Marco Metzger ◽  
Lothar Just ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Flow Rate ◽  
Fluid Intake ◽  
Salt Intake ◽  
Control Diet ◽  
High Salt ◽  
Urinary Flow Rate ◽  
Urinary Flow ◽  
High Salt Intake

Serum- and glucocorticoid-inducible kinase (SGK1) is transcriptionally upregulated by mineralocorticoids and activated by insulin. The kinase stimulates the renal epithelial Na+ channel and may thus participate in blood pressure regulation. Hyperinsulinemia is triggered by dietary fructose, which sensitizes blood pressure for salt intake. The role of SGK1 in hypertensive effects of combined fructose and high-salt intake was thus explored in SGK1 knockout mice ( sgk1−/−) and their wild-type littermates ( sgk1+/+). Renal SGK1 transcript levels of sgk1+/+ mice were significantly elevated after fructose diet. Under control diet, fluid intake, urinary flow rate, urinary Na+, K+, and Cl− excretion, and blood pressure were similar in sgk1−/− and sgk1+/+ mice. Addition of 10% fructose to drinking water increased fluid intake and urinary flow rate in both genotypes, and did not significantly alter urinary Na+, K+, and Cl− output in either genotype. Additional high NaCl diet (4% NaCl) did not significantly alter fluid intake and urine volume but markedly increased urinary output of Na+ and Cl−, approaching values significantly ( P < 0.05) larger in sgk1−/− than in sgk1+/+ mice (Na+: 2,572 ± 462 vs. 1,428 ± 236; Cl−: 2,364 ± 388 vs. 1,379 ± 225 μmol/24 h). Blood pressure was similar in sgk1+/+ and sgk1−/− mice at control diet or fructose alone but increased only in sgk1+/+ mice (115 ± 1 vs. 103 ± 0.7 mmHg, P < 0.05) after combined fructose and high-salt intake. Acute intravenous insulin infusion (during glucose clamp) caused antinatriuresis in sgk1+/+ mice, an effect significantly blunted in sgk1−/− mice. The observations reveal a pivotal role of SGK1 in insulin-mediated sodium retention and the salt-sensitizing hypertensive effect of high fructose intake.

Developing essential hypertension: a syndrome involving ANF deficiency?

1991 ◽  
Vol 69 (10) ◽  
pp. 1582-1591 ◽  
Author(s):  
P. Weidmann ◽  
P. Ferrari ◽  
Y. Allemann ◽  
C. Ferrier ◽  
S. G. Shaw
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Cyclic Gmp ◽  
Vascular Reactivity ◽  
Salt Intake ◽  
Deficiency Syndrome ◽  
Left Ventricular ◽  
High Salt ◽  
Cardiac Complications ◽  
High Salt Intake

The pathogenesis of essential hypertension may possibly involve a deficiency in, or a decreased response to, endogenous vasodilator and natriuretic factor(s). Searching for hereditary or familial defects, it is plausible to evaluate blood pressure (BP) regulating factors in (yet) normotensive offspring of hypertensive parents (OHyp), some of whom are in fact in a stage of prehypertension. Studies by our group demonstrated that compared with healthy offspring of normotensive parents, OHyp have plasma atrial natriuretic (ANF) factor levels that are unaltered on a low salt intake but often fail to increase normally in response to a high salt intake. Plasma levels of cyclic GMP, the presumed second messenger of ANF, also may tend to be decreased in certain OHyp. On the other hand, renal excretory responses of cyclic GMP and electrolytes to ANF infused in "physiological" dose were unchanged in some OHyp tested so far. In borderline to moderate, uncomplicated essential hypertension, plasma ANF levels are often "normal." This may be inappropriately low relative to the existing BP, although the relationship of circulating ANF to atrial pressures in essential hypertension remains to be clarified. A conversion to higher plasma ANF values may occur with cardiac complications such as left ventricular hypertrophy, enlargement, dysfunction, or overt heart failure. Acute or short-term elevation of circulating ANF within the physiological and pathophysiological range by ANF infusion produces an exaggerated natriuresis and lowers BP in essential hypertensive patients. We postulate a syndrome of ANF deficiency, characterized by an impaired response of circulating ANF to high salt intake and by low cyclic GMP levels in certain yet normotensive offspring of essential hypertensive parents and by inappropriately "normal" plasma ANF in some patients with uncomplicated essential hypertension. At the stage of prehypertension, a disturbance in the ANF – cyclic GMP pathway may be expressed primarily at the circulatory rather than at the renal level. Hypertension-prone humans also tend to have an exaggerated vascular reactivity to norepinephrine. Whether the two disturbances may be interrelated is presently unknown. Both defects may potentially predispose to the development of essential hypertension. Relative ANF deficiency, an enhanced natriuretic response to ANF, and a sustained antihypertensive effect of infused ANF may represent a rational basis for treatment of essential hypertension with agents that activate the ANF system.Key words: offspring of hypertensive parents, essential hypertension, ANF, ANF deficiency syndrome, cyclic GMP, blood pressure regulation, vascular reactivity, renal function.

scholarly journals Effects of High Salt Intake on Blood Pressure and Cardiovascular Disease: The Role of COX Inhibitors

2016 ◽  
Vol 39 (4) ◽  
pp. 240-242 ◽  
Author(s):  
Steven G. Chrysant
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Salt Intake ◽  
High Salt ◽  
Cox Inhibitors ◽  
High Salt Intake

scholarly journals High salt intake: detrimental not only for blood pressure, but also for bone health?

Endocrine ◽  
2015 ◽  
Vol 49 (3) ◽  
pp. 580-582 ◽  
Author(s):  
Thomas Remer
Keyword(s):  
Blood Pressure ◽  
Bone Health ◽  
Salt Intake ◽  
High Salt ◽  
High Salt Intake

Increased depressor response to N-arachidonoyl-dopamine during high salt intake: role of the TRPV1 receptor

2007 ◽  
Vol 25 (12) ◽  
pp. 2426-2433 ◽  
Author(s):  
Youping Wang ◽  
Donna H Wang
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Trpv1 Receptor ◽  
Depressor Response ◽  
High Salt Intake

Abstract 142: A Fructose-but Not a Glucose-enriched Diet, Induces a Salt-dependent Increase in Blood Pressure and Enhances NKCC2 Phosphorylation in Normal Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Keyona N King-Medina ◽  
Emily Henson ◽  
Pablo Ortiz
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Salt Intake ◽  
Caloric Intake ◽  
High Salt ◽  
Human Consumption ◽  
Thick Ascending Limb ◽  
Sprague Dawley ◽  
High Fructose ◽  
High Salt Intake

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.

scholarly journals The Relationship Between Urine Uromodulin and Blood Pressure Changes: The DASH-Sodium Trial

2020 ◽  
Author(s):  
Christine Y Bakhoum ◽  
Cheryl A M Anderson ◽  
Stephen P Juraschek ◽  
Casey M Rebholz ◽  
Lawrence J Appel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Control Diet ◽  
Random Order ◽  
High Salt ◽  
Thick Ascending Limb ◽  
Feeding Period ◽  
High Sodium ◽  
Sodium Diet ◽  
High Salt Intake

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.

scholarly journals Relationship Between Salt Intake and Blood Pressure in Hypertensive Patients in Beijing

2020 ◽  
Vol 33 (4) ◽  
pp. 371-371
Author(s):  
Hong-yi Wang ◽  
Yong-jie He ◽  
Wei Li ◽  
Fan Yang ◽  
Ning-ling Sun
Keyword(s):  
Blood Pressure ◽  
Ambulatory Blood Pressure ◽  
Salt Intake ◽  
Blood Pressure Monitoring ◽  
Urinary Sodium Excretion ◽  
High Salt ◽  
Pressure Monitoring ◽  
Hypertensive Patients ◽  
High Salt Intake ◽  
Tertiary Hospitals

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.

scholarly journals High Salt Intake Augments Blood Pressure Responses During Submaximal Aerobic Exercise

2020 ◽  
Vol 9 (10) ◽  
Author(s):  
Matthew C. Babcock ◽  
Austin T. Robinson ◽  
Kamila U. Migdal ◽  
Joseph C. Watso ◽  
Christopher R. Martens ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Aerobic Exercise ◽  
Salt Intake ◽  
High Salt ◽  
High Salt Intake ◽  
Submaximal Aerobic Exercise ◽  
Blood Pressure Responses

scholarly journals Mechanisms for Linking High Salt Intake to Vascular Tone: Role of Na+ Pump and Na+/Ca2+ Exchanger Coupling

2010 ◽  
Vol 130 (11) ◽  
pp. 1399-1405 ◽  
Author(s):  
Satomi KITA ◽  
Takahiro IWAMOTO
Keyword(s):  
Vascular Tone ◽  
Salt Intake ◽  
High Salt ◽  
High Salt Intake
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